Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal 2 > Robbins Ch. 20 - Glomerular Disease > Flashcards

Robbins Ch. 20 - Glomerular Disease Flashcards

1
Q

Selective vs. non-selective proteinuria

A

Selective = albumin ONLY

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

Multiple bands on serum protein electrophoresis (IgG and Kappa regions)

A

Multiple myeloma

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

Differential Dx for edema

A
  • Kidneys
  • Heart (perfusion)
  • Liver (protein synth)
  • GI (protein absorption)
  • Lungs (fibrosis)
  • Other
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

4 compartments of kidney

A
  • Glomeruli
  • Tubules
  • Interstitium
  • Vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

See Bence-Jones proteinuria, think ____

A

Tubular pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Light chains of Ig’s deposited in proximal tubules

A

Myeloma kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Azotemia

A

Increased serum BUN and creatinine via decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prerenal azotemia

A

Hypoperfusion of kidneys (hemorrhage, shock, volume depletion, CHF) –> azotemia

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

Post-renal azotemia

A

Obstruction distal to kidney –> azotemia

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

Uremia

A

Azotemia + other clinical findings and biochemical abnormalities due to renal damage

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

Rapid decline in GFR

A

Acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

See acute kidney injury (AKI), think damage to ______

A

ANY of the 4 areas

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

Definition of chronic kidney disease

A
  • Diminished GFR (
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Severe CKD can present as?

A

Uremia

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

Definition of end stage renal disease (ESRD)

A

GFR

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

Typical presentations of glomerular disease (6)

A
  • Nephritic syndrome
  • Nephrotic syndrome
  • Asymptomatic hematuria or proteinuria
  • Chronic renal failure (CKD)
  • Acute renal failure (AKI)
  • Renal tubular defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Typical presentations of tubulointerstitial disease (6)

A
  • Acute renal failure (AKI)
  • Renal tubular defects
  • UTI
  • Urinary tract obstruction
  • Renal tumors
  • Nephrolithiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nephrotic syndrome

A 
Proteinuria (> 3.5 g/day)
Hypoalbuminemia
Severe edema
Hyperlipidemia
Lipiduria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nephritic syndrome

A

Hematuria
Azotemia
Oliguria
Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rapidly progressive glomerulonephritis (RPGN)

A

Nephritic syndrome
Rapid decline in GFR
Crescent formations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Isolated urinary abnormalities

A
  • Microscopic hematuria
    AND/OR
  • Subnephrotic proteinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chronic renal failure (CKD)

A

Azotemia –> uremia (over several months)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does the glomerulus respond to injury?

A
  • Hypercellular (proliferation)
  • Basement membrane thickening
  • Hyalinosis (protein deposition) and sclerosis (matrix)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hypercellular response to glomerular injury

A
  • Mesangial/endothelial proliferation
  • Leukocyte infiltration
  • Crescent (epithelial cell) formations in urinary space (RPGN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Basement membrane thickening in glomerular injury
Electron-dense deposits (immunologic) - Ag-Ab complex depositions - In situ reactions to Ag's in BM
26
In situ reactive feature of BM
Collagen type 4
27
Most common SYSTEMIC diseases w/ glomerular involvement
- SLE | - DM
28
See glomerular disease + pulmonary bleeding... | Think ______
- Goodpasture syndrome (anti-BM Ab's) | - Wegener granulomatosis
29
See nephrotic syndrome... | Think ______
- Membranous glomerulopathy (adult) - Minimal-change disease (child) - FSGS (adult)
30
See IgA nephropathy... | Think ______
- Recurrent hematuria or proteinuria - Henoch-Schonlein purpura (renal + skin + viscera) - Berger disease (renal IgA nephropathy)
31
See mixed nephrotic/nephritic pattern... | Think ______
- Dense deposit disease (MPGN type 2)
32
HEREDITARY glomerular diseases
- Alport syndrome | - Thin basement membrane disease
33
See subepithelial deposits... | Think ______
- Acute glomerulonephritis
34
See epimembranous deposits... | Think ______
- IN SITU complex deposition (Heymann) - Membranous nephropathy - Dense deposit disease
35
See subendothelial deposits... | Think ______
- CIRCULATING complex deposition - Lupus nephritis - MPGN
36
See mesangial deposits... | Think ______
- Acute proliferative glomerulonephritis (IgG, C3 deposits) | - IgA nephropathy (IgA deposits)
37
2 types of ANTIBODY-mediated glomerular injury
- In-situ complex deposition | - Circulating complex deposition
38
2 types of IN-SITU complex deposition
- Fixed, intrinsic antigen (glomerular BM, other) | - Planted antigen
39
2 types of CIRCULATING complex deposition
- Endogenous antigens | - Exogenous antigens (drugs, organisms)
40
Other 2 types of glomerular injury besides Ab-mediated
- Cell-mediated | - Alternate complement-mediated
41
See basement membrane deposits... | Think ______
- IN-SITU complex deposition (intrinsic Ag) - Anti-GBM - Goodpasture syndrome
42
Progression to ESRF presents with what 2 features?
- FSGS | - Tubulointerstitial fibrosis
43
Acute proliferative glomerulonephritis Pathology presentation
Immune complex glomerular injury due to EXOGENOUS antigen - Hypercellularity (completely full glomerulus on histo) - Leukocyte infiltration (exudate in glomerular tuft) - SubEPITHELIAL deposits - GRANULAR IgG and C3 in mesangium
44
Acute proliferative glomerulonephritis: Patient presentation
- Sick Child (6-10 y/o) - Previous throat or skin infection - Dysmorphic red cells or RBC casts - Periorbital edema - Oliguria, hematuria, mild proteinuria, mild HTN
45
Typical cause of acute proliferative glomerulonephritis
Streptococcal (Beta-hemolytic strep) infection
46
Confirm diagnosis of post-strep APGN
ASO titer --> SpeB
47
Treatment of post-strep APGN
Water and salt restriction | NOT antibiotics
48
See nephritic syndrome... | Think _______
- Acute proliferative (post-infection) glomerulonephritis | - Rapidly progressive glomerulonephritis
49
Pathologic differences between APGN and RPGN
RPGN = CRESCENTS, chronic glomerulosclerosis over time
50
Linear deposits of IgG and C3 in the GBM
Type 1 RPGN
51
Linear deposits of IgG and C3 in GBM | Pulmonary hemorrhage
Goodpasture syndrome (anti-BM Ab's)
52
Genetic predisposition to RPGN/goodpasture
HLA-DRB1
53
Treatment for type 1 RPGN
Plasmapheresis (to remove circulating antibodies)
54
Causes of type 2 RPGN What type of APGN can progress to RPGN?
- Acute proliferative glomerulonephritis - Lupus nephritis - IgA nephropathy - Henoch-Schonlein purpura ADULTS with it, NOT kids
55
Type 1 vs. type 2 RPGN
Type 1 = Anti-GBM antibody, LINEAR deposits | Type 2 = Immune complex deposition, GRANULAR deposits
56
Treatment for type 2 RPGN
Treat underlying disease (NOT plasmapheresis)
57
Dx of type 3 RPGN
- No anti-GBM antibodies or immune complexes | - Circulating ANCAs
58
Only nephrotic syndrome disease with NO hematuria
Minimal change disease
59
Common pathologic feature of nephrotic syndrome diseases
FOOT PROCESS FUSION
60
MOST COMMON systemic causes of nephrotic syndrome
- Diabetes mellitus | - SLE
61
Primary membranous glomerulopathy: Genetic causes/factors
- HLA-DQA1 | - Anti-PLA2R antibodies
62
Membranous glomerulopathy: Pathology presentation
- BM (or capillary wall) thickening w/in glomerulus - Epimembranous/subepithelial GRANULAR IgG deposits (SPIKE AND DOME) - Effaced/fused foot processes
63
Minimal change disease: Patient presentation
- SEVERE EDEMA - CHILD - Previous viral respiratory infection or immunization - SELECTIVE proteinuria (albuminuria)
64
Minimal change disease: Pathology presentation
- Foot process fusion | - Lipiduria
65
Patients with minimal change disease can tend to also develop ______
Hodgkin (B-cell) lymphoma
66
Treatment of minimal change disease (MCD)
Corticosteroids (VERY responsive)
67
Pathophysiology of nephrotic syndrome
- Ab's against epithelial (podocyte) antigens - Injury via cytokines, etc. - Foot process fusion + detachment - Defective GBM and filtration slits --> proteinuria
68
Patient presentation in FSGS vs. MCD
- ADULT - Severe edema - Hematuria, reduced GFR, HTN - NON-SELECTIVE proteinuria - POOR response to corticosteroids - Significant progression to CKD
69
HIV-infected individual with glomerular disease
FSGS "collapsing variant"
70
MAJOR pathologic difference for FSGS
IgM, NOT IgG
71
See nephrotic/nephritic mix... | Think ______
Membranoproliferative glomerulonephritis
72
MPGN: Pathology presentation
- GBM thickening and splitting - MESANGIAL cell proliferation --> SPLITS GBM - Leukocyte infiltration - Accentuation of LOBULAR architecture
73
MPGN type 1 vs. type 2: Pathology
Type 1 = Subendothelial deposits, IgG + C3 | Type 2 = Intra-GBM deposits, C3 ONLY
74
Primary MPGN type 1: Patient presentation
- Child or young adult w/ proteinuria (nephrotic) - Microscopic hematuria (nephritic features) - Mild HTN - Progression to chronic renal failure (50%) over years
75
Secondary MPGN type 1: Patient presentation
- Adult - Chronic antigenemia (infection, autoimmune, neoplasia) - Progression to chronic renal failure (50%) over years
76
Causes of antigenemia in secondary MPGN type 1
- Hep C - SLE endocarditis - CLL, lymphoma, melanoma - Neoplasia/cancer
77
MPGN type 2: Patient presentation
- Child - PRIMARY disease - Hematuria (nephritic syndrome) - Severe renal disease - Poor prognosis - Recurrence following renal transplantation
78
Deposits in MPGN type 2
C3NeF ("nephritic factor") = IgG autoAb that binds C3 convertase and ACTIVATES ALTERNATIVE PATHWAY
79
IgA nephropathy: Pathology presentation
- IgA deposits in mesangium | - Mesangial proliferation and matrix increase
80
Child/young adult (10-30) Male, causasian or asian Red/purple blotches on abdomen and buttox Recurrent hematuria (NO PROGRESSION of renal disease) Previous URI or visceral infection
Henoch-Schonlein purpura (IgA nephropathy)
81
Patients with HSP are known to be at risk for _____
Gluten enteropathy and liver disease
82
Most likely glomerular diseases to progress to CGN
1. Crescentic GN (RPGN) 2. FSGS 3. MPGN 4. Membranous nephropathy / IgA nephropathy 5. Acute proliferative glomerulonephritis
83
Chronic glomerulonephritis
- DIFFUSE, GLOBAL glomerular disease | - Commonly with NO Dx'd antecedent glomerulonephritis
84
See FHx of hematuria or recurrent in childhood... | Think _____
- Alport syndrome | - Thin basement membrane disease
85
Alport syndrome
- IRREGULAR thickened BM ("moth eaten" or "frayed") | - Vision issues
86
Thin Basement Membrane Disease
- Hematuria via thinned glomerular BMs | - Mutation in collagen type 4
87
Secondary renal diseases (systemic diseases) that present with NEPHROTIC syndrome/PROTEINURIA
- Diabetic neuropathy - Hepatitic C (MPGN type 1) - HIV (FSGS)
88
Secondary renal diseases (systemic diseases) that present with NEPHRITIC syndrome/HEMATURIA
- SLE - Bacterial endocarditis (APGN) - Goodpasture (RPGN) - HSP (IgA nephropathy)
89
What percentage of ESRD is due to diabetic nephropathy? What percentage of DM patients progress to ESRD?
30% 40%
90
Processes involved in formation of diabetic glomerular lesions
- Metabolic defect in hyperglycemia --> thickened GBM | - Hemodynamic effects from glomerular hypertrophy --> glomerular sclerosis
91
Microscopic pathology of diabetic kidney
1. DIFFUSE THICKENING OF BMs (tubular and glomerular) 2. Mesangial matrix sclerosis --> compressed capillaries 3. Nodular glomerulosclerosis (PAS-positive) 4. Thickened, HYALINIZED arterioles
92
Nodular glomerulosclerosis
Diabetic glomerulosclerosis
93
Kimmelstiel-Wilson Disease
Diabetic glomerulosclerosis
94
Gross pathology of diabetic kidney
- Diffuse granular, pitted surface | - Thinning of renal cortex
95
Those with diabetic kidney are at risk for what? Evidenced how?
Secondary infections Irregular cortical depressions 2º to pyelonephritis
96
Does diabetic nephropathy generally affect large or small vessels?
SMALL
97
SLE nephritis
- Subendothelial IgG dense deposits ("WIRE LOOPS") | - Hyperproliferation of glomerulus

Renal 2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions