Brainscape's Knowledge GenomeTM

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


See full index

Renal 2 > Robbins, Chapter 20, The Kidney > Flashcards

Robbins, Chapter 20, The Kidney Flashcards

1
Q

Azotemia definition.

Its extra-renal sources (2)

A

Biochemical abnormality indicating an elevation of blood urea nitrogen (BUN) and serum creatinine levels.

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

Azotemia associated with increased or decreased GFR?

A

Decreased

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

What is prerenal azotemia? Is there parenchymal damage?

Prerenal azotemia occurs after what state of kidney perfusion?

A

Occurs after HYPOPERFUSION of kidneys in the ABSENCE of parenchymal damage.

**The prostatic hyperplasia could lead to obstructive uropathy with bilateral hydronephrosis, renal cortical atrophy, and eventual chronic renal failure.

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

Examples of what causes prerenal azotemia.

A

Due to HEMORRHAGE, SHOCK, VOLUME DEPLETION, CHF.

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

When is postrenal azotemia seen?

A

When urine outflow is obstructed distal to calyces and renal pelvis.

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

What corrects postrenal azotemia?

A

Removal of obstruction.

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

What is it called when azotemia becomes associated with a constellation of clinical signs and symptoms and biochemical abnormalities?

A

Uremia

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

What are common secondary manifestations that characterize uremia (3)?

A

GI - uremic gastroenteritis
Peripheral nerves - peripheral neuropathy
Heart - uremic fibrinous pericarditis

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

Nephritic Syndrome due to?
How do these patients present? (i.e. sick or non-sick)
Associated with what clinical manifestations?
Most common cause?

A

-Caused by glomerular disease&raquo_space; ACUTE GLOMERULONEPHRITIS.
-Present as sick with acute onset of HEMATURIA, azotemia, oliguria with azotemia, proteinuria, HTN, possible fever
also - with dysmorphic red cells and red casts, mild to moderate proteinuria
-Commonly caused by immunologically mediated glom injury

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

Nephrotic Syndrome due to?
How do patients present? (i.e. sick or non-sick)
Associated with what clinical?

A

-Caused by glom disease.
-Present not as sick as nephritic patients.
Characterized by heavy proteinuria of more than 3.5g/day
also - hypoalbuminemia, hyperlipidemia, lipiduria, edema

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

What is heavy proteinuria level?

A

More than 3.5g/day

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

Acute glomerular response to injury

A

HYPERCELLULARITY with proliferation of mesangial and/or endothelial cells, influx of leukocytes, formation of CRESCENTS

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

Chronic glomerular response to injury

A

Basement membrane thickening

Hyalinosis and sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diffuse primary glomerulonephropathy

Focal primary glomerulonephropathy

A

Diffuse - Involve all of a kidney’s gloms, in their entirety.
Focal - Involves a subset of the gloms in the kidney

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

Global primary glomerulonephropathy

Segmental primary glomerulonephropathy

A

Global - Involves all of an individual glom.

Segmental - Only a portion of the affected gloms are involved.

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

Capillary loop or mesangial primary glomerulonephropathy

A

Affecting predominanty capillary or mesangial regions.

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

What mechanism underlies most primary glomerulopathy and secondary glomerular disorders?

A

Immune!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ESRD has GFR of what?

A

less than 5% of normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of syndrome with clinical manifestations of:
Glomerular syndrome.
Acute nephritic, proteinuria, acute renal failure

A

Rapidly Progressive Glomerulonephritis (RPGN)

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

Chronic Renal Failure:
What type of syndrome?
What clinical manifestations?
Time frame.

A

Glomerular syndrome.

Azotemia, progressing to uremia for months to years.

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

Isolated Urinary Abnormalities

A

Glomerular (micro) hematuria and/or subnephrotic proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Response of glom to injury (3).

A

Hypercellularity (severe = crescents), BM thickening, hyalinosis and sclerosis

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

A SUBEPITHELIAL HUMP is found in the glom - what is it indicative of?

A

Acute glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

An EPIMEMBRANOUS DEPOSIT is found in the glom - what is it indicative of?

A

Membranous nephropathy or Heymann glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

A SUBENDOTHELIAL DEPOSIT is found in the glom - what is it indicative of?

A

Lupus nephritis

Membranoproliferative glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MESANGIAL DEPOSITS are found in the glom - what is it indicative of?

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most common form of antibody mediated glomerulonephritis is caused by what two types of immune complex formation?
What pattern of deposition is seen upon immunofluorescence?

A

Formation of immune complexes:
- Endogenous antigens - PLA2R in membranous nephropathy
- Exogenous antigens - microbial.
GRANULAR pattern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Anti-GBM antibody mediated disease PATTERN OF DEPOSITION seen upon immunofluorescent staining.
Where is the deposition in the glom?

A

LINEAR pattern.

In Situ deposits on the BM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Heymann glomerulonphritis deposition is where in the glom?

A

In Situ deposition on foot processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

FSGS and tubulointerstitial fibrosis are two major histological features of what?

A

PROGRESSIVE renal damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the principal glomerular manifestation of progressive renal injury? What does it eventually lead to?

A

Focal Segmental GlomerularSclerosis

Leads to global glomerular involvement and glomerular obsolescence. &raquo_space;» ESRD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What accompanies progressive glom injury (FSGS) in other renal structures?

A

tubulointerstitial fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What am I?

Diffuse proliferation of glomerular cells with presence of leukocytes.

A

Acute Proliferative Glomerulonephritis/Post Strep Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What am I?
Bug - post-strep A beta-hemolytic Strep, 1-4 weeks after
Antibody forms against M protein Antigen (**ASO titer elevated).
Immune response results in ACUTE NEPHRITIC SYNDROME.
Type III hypersensitivity

A

Acute Proliferative Glomerulonephritis/Post Strep Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q 
What am I?
LM - Gloms are enlarged and HYPERCELLULAR, tubules contain RED CELL CASTS
IF - GRANULAR deposits of IgM, IgG, C3
EM - "lumpy bumpy" on subepithelial side
NEUTS in lumen
A

Acute Proliferative Glomerulonephritis/Post Strep Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What am I and how do you treat?
A young child, 6-10 yo with malaise, fever, nausea, HEMATURIA, periorital edema. Possible facial rash.
1-2 weeks after pharyngeal and/or cutaneous infection. Elevated ASO titer.

A

Acute Proliferative Glomerulonephritis/Post Strep Glomerulonephritis.
Treat with fluid/electroyte therapy and 95% recover well. 1% develop RPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What infections other than group A strep can induce Acute Proliferative Glomerulonephritis?

A

bacterial (strep pneumo), Viral (Hep B, Hep C, HIV), Parasitic (toxo, malaria)

38
Q

How does the course of Acute Proliferative Glomerulonephritis differ in ADULTS v. CHILDREN? What may ADULTS (not children) progress to?

Treatment of children?

A

95% of children recover completely. Adults have more aggressive and atypical - only 60% recover completely. ADULTS may progress to RPGN II

Children - treat with fluid/electrolyte therapy

39
Q

What am I?
Nephritic Syndrome
Severe glomerular injury associate with formation of crescents in most glom and not necessarily associated with one syndrome.

A

Rapidly Progressive Glomerulonephritis: Definition

40
Q

RPGN: Pathogenesis - types (3) and each type’s immunological findings. Which is most common? Which is primary?

A

Type 1 - anti-GBM (Goodpastures, anti-collagen type 4)
Type 2 - Immune Complex (postinfectious, SLE, Henloch-Schloen)
Most common and PRIMARY: TYPE 3 - Pauci Immune (associated with p- or c-ANCA; Wegner’s)

41
Q

What am I?
Histo - CRESCENTS within BOWMAN’S SPACE
EM - wrinkled and ruptured BM

Immunofluorescence:
T1 = LINEAR IgG, 
T2 = Granular
T3 = no anti-GMB ab or immune complexes but have circulating ANCA
Gross - enlarged, pale kidneys
A

RPGN

42
Q

What am I? and what tx? What is the prognosis
Present with hematuria, red cell casts, and proteinuria approaching nephrotic ranges, possible HTN and edema. (1) anti-GBM and recurrent hemoptysis (2) immune complex (3) ANCA

A

RPGN

(1) Goodpastures, Type I Cresentic
(2) SLE, HSP, post infectious
(3) Idiopathic RPGN, Type III Cresentic

Treatment - (1) = plasmapheresis; Type 2, 3=does not respond to plasmapheresis - use anti inflammatory

Prognosis - not good

43
Q

RPGN I patients found to have HLA subtypes have higher prevalence of what? And recurrent hemoptysis. Rapid progression to renal failure.

A

Goodpastures

44
Q

What is the primary renal disease where IgA deposits are found in the mesangium detected by immunofluorescence?

A

IgA nephropathy

45
Q

What is the difference between a primary renal disease v. secondary? More frequent in children or adults?

A

Primary - only kidney affected, no systemic disease. Most common cause of nephrotic syndrome in children.
Secondary - systemic disease that CAUSE renal/nephrotic diseaes (like DM or SLE). Secondary causes of nephritic syndrome more frequent in adults (about 40% of cases)

46
Q

Nephrotic Syndrome - what causes it, what leaks, what happens to colloid pressure, what are the clinical manifestations?

A

Initial event causes DERANGEMENT OF GLOMERULAR CAPILLARIES with increased permeability to protein, PROTEINURIA results&raquo_space; hypoalbuminuria and decreased colloid pressure
EDEMA (periorbital and peripheral)
HYPERLIPIDEMIA

47
Q

Membranous Glomerulopathy - nephritic or nephrotic and in what % of people with membranous glom?
What % are primary and more common in adults of kids?
What genetics - alleles and antibodies are involved?

A

Nephrotic - 85%
75% primary - most common cause of nephrotic syndrome in adults
HLA alleles and antibodies to renal autoantigen PLA2 receptor with roles for complement (primarily MAC and IgG4

48
Q

Does Primary Membranous Glomerulopathy respond well to corticosteroid treatment?
Does Secondary MG (secondary to autoimmune disease)?

A

No

Possibly

49
Q

What is this the definition of?
Diffuse thickening of glom capillary wall with accumulation of electron dense immunoglobulins with deposits on subepithelial side of BM. Effaced food processes.

A

Definition of Membranous Glomerulopathy

50
Q

What has a pathogenesis of chronic immune complex deposition? Most common in adults.
Associated with antibody mediated (THYROIDITIS), penicillamine, lupus, HEPATITIS B/C, gold/mercury, schisto.

A

Membranous Glomerulopathy

51
Q

What has:
LM - uniform diffuse THICKENING of BM with thick CAPILLARY LOOPS
EM - dense deposits of IgG in subEPITHELIAL, forming “SPIKES” which form DOMES
IF - GRANULAR IgG and C3
-Effaced Foot processes

A

membranous glomerulopathy

52
Q

Is proteinuria selective or non selective in Membranous Glomerulopathy? And it persists in what percentage of patients?
Prognosis: % develop renal insufficiency, % progress to ESRF

A

Non-selective (large and small proteins). Persists in 60% of patients.
40% renal insuff
10% ESRF

53
Q 
MCD
Age range 
Onset (follows what?) 
Presenting clinical sign
The only thing seen on biopsy
A

KIDS! 2-6yo
Follows a respiratory infection
Edema
Biopsy - Foot Process Fusion. All other normal LM glom.

54
Q

Is MCD effectively treated by corticosteroids?

A

Yes

55
Q

MCD is associated with what type of cancer?

A

Hodgkins lymphoma

56
Q

MCD has what type of proteinuria?

A

SELECTIVE

57
Q

MCD has was type of prognosis?

A

Excellent

58
Q

Massive proteinuria despite preservation of renal function without hematuria or HTN.
LM and IF = SEE NOTHING
EM = see PODOCYTE FUSION/EFFACEMENT

A

Clinical course of MCD and findings

59
Q

What am I?
Sclerosis of some, but not all glomeruli.
Affecting only part of each affected glomeruli.
With nephrotic syndrome.
Adults, even with steroids have a poor prognosis.
Also associated with African-Americans, loss of renal tissue, sickle cell, heroin, AIDS, obesity

A

Focal Segmental GomeruloSclerosis

60
Q

Does FSGS respond to corticosteroids?

Does it remit spontaneously?

A

No

No

61
Q

Does primary FSGS primarily affect adults or children?
Do children or adults have better prognosis?
What two races have greatest incidence?

A

Adults (35% of those with Nephrotic Syndrome) > Children (10% of those with Nephrotic Syndrome
Children
Hispanics and Blacks

62
Q

APOL1 on ch22 strongly associated with resistance to trypanosome infection - associated with what race and increased incidence of what nephrotic syndrome?

A

Those of African descent.

FSGS

63
Q

FSGS or MCD?

  1. Higher incidence of hematuria, reduced GFR, HTN
  2. Nonselective proteinuria
  3. Poor response to corticosteroids
  4. Progression of CKD, at least 50% developing ESRD within 10 years
A

FSGS

64
Q

What infection is associated with the collapsing variant of FSGS? What does this mean?
How does this differ from idiopathic FSGS?

A

HIV associated, esp in African Americans. Complete glom collapse.
EM - This type has large presence of tubuloretucular inclusions within endothelial cells.

65
Q

NPGS1, NPGS2, TPRC6, alpha-actinin 4 mutations localize to where? what does PPGS2 result in?

A

Podocyte slit diaphragms.

NPGS’s code for nephrin. NPGS2 results in nephrotic syndrome in children.

66
Q

What am I?
LM = parts of some glom are eosinophilic(pink) with sclerosis.
EM = effacement of podocytes, as in MCD
IF = IgM and C3 in sclerotic areas

Glomerulosclerosis and increased matrix synthesis are due to genetic defects or circulating cytokines of the slit diaphragm.

A

FSGS

67
Q

An adaptive response to loss of renal mass. What is progressive FSGS called - it occurs after removal of diseased or healthy nephrotic segment caused by hypertrophy of remaining segment.

A

Renal Ablation FSGS

68
Q

Is Membranoproliferative GN nephrotic or nephritic?

A

Mixed

69
Q

What is the difference between type I and type II MPGN?

A

I=immune complex deposition and activation IgG and complement
II=DDD, a C3 glomerulopathy - autoantibody: alternative complement pathway

70
Q

If C3 is low in serum, what GN is it? The ONLY glomerular disease with changed serum complement.

A

MPGN

71
Q

What am I?
LM=TRAM-TRACK appearance of glom BM
EM=nonspecific, type II has dense deposits
IF = granular C3 pattern

A

MPGN

72
Q

What MPGN type has a circulating (C3NeF) C3 NEPHRITIC FACTOR? What does this bind to and what does it do?

A

MPGN II. IgG autoantibody that binds to the alternative pathway C3 convertase and leads to continuous activation of the pathway» C3 will be low!

73
Q

What am I?
Basement membrane thickening, increased mesangial matrix, accentuation of lobular architecture, influx of neuts, mesangial cell proliferation.

A

MPGN

74
Q

What is “tram-track” in MPGN I and II?

A

mesangial proliferation and inrceased mesangial matrix that may dissect and split the glom BM

75
Q

What am I?
Normally in children, with nephrotic syndrome presentation. Microscopic hematuria, with additional nephritic features (HTN, oliguria, edema, renal insufficiency).
50% develop chronic renal failure over 10 years
Tx with steroids is NOT beneficial.

A

MPGN I, Primary

76
Q

What else does MPGN Type I resemble with slow progression, crescents, and unremitting course?

A

RPGN

77
Q

What am I?
Exclusively adults. Chronic antigenemia association.
Also associated with: Hep C with CRYOGLOBULINEMIA, SLE, hep B, chronic visceral abscesses, HIV, schisto, malignancies (CLL, lymphoma, melanoma).

Dismal prognosis.

A

MPGN I, Secondary

78
Q

Although mixed, which MPGN has hematuria as a more dominant clinical finding?
Although mixed, which MPGN has proteinuria as a more dominant clinical finding?

A

Hematuria in virtually ALL - MPGN II

Proteinuria - MPGN I

79
Q

Does MPGN I or II have a poorer prognosis/mroe severe renal disease?
Which has a more frequent recurrence following renal transplant?
What has extremely dense deposits?

A

MPGN II

80
Q

IgA Nephropathy - nephritic or nephrotic?

A

nephritic

81
Q 
What am I?
LM= MESANGIAL proliferation/WIDENING
EM=nonsepcific
IF=GRANULAR IgA in mesangium
Which MUST be used to diagnose?
A

IgA nephropathy

IF

82
Q

What is the most common cause of glomerulonephritis worldwide?

A

IgA Nephropathy

83
Q

What do Berger Disease and Henoch Schonlein purpura have in common (immunologically)?
What makes them different?

A

both are IgA nephropathies
Bergr is a renal localized IgA neph
HSP is a systemic disease, associated with systemic vasculitis

84
Q

What am I?
Most common nephropathy world wide. Fairly benign/PAINLESS, BRIGHT RED BLEEDING in urine, follows an URI, GI infection, or UTI. RECURRENT episodes of hematuria without progression of renal disease in majority of patients, but CRF in 15-40% as a slowly progressive disease over 20 years (benign, but can progress to renal failure)

A

IgA nephropathy

85
Q

What is IgA nephropathy?

primary or secondary, what deposits, detected by what?

A

Primary renal disease where IgA deposits in mesangium, detected by immunofluorescnence.

86
Q

What am I?
Most common in children and YA (2nd-3rd decades). Caucasians and Asians, Males>Females. 1st degree relative family hx. Known association with celiac’s/GLUTEN ENTEROPATHY and LIVER DISEASE.

A

IgA Nephropathy

87
Q 
These lead to what? 
90% RPGN (crescentic)
50-80% FSGS
50% MPGN
30-50% IgAN, Membranous nephropathy
1-2% post strep GN
A

Chronic glomerulonephritis

88
Q

What is the endpoint of all nephrotic and nephritic syndromes?

A

Chronic glomerulonephritis

89
Q

What is characterized by EXTENSIVE HYALINIZATION and FIBROSIS of glom (lg amt of collagen on trichrome stain)?
Kidneys have diffiselu granular surfaces and thinned cortex. Glom completely effaced by hyalinized CT, marked tubular atrophy. Possible changes due to dialysis.

A

Chronic glomerulonephritis

90
Q

In chronic glomerulonephritis, HTN is often comcomitant with CRF, so what is often present as well?

A

arteriole sclerosis

91
Q

What does CRF inevitably lead to?

A

UREMIA (pericarditis, uremic gastroenteritis, secondary hyperPTH with nephrocalcinosis and renal osteodystrophy)
with HTN, edema, dialysis, death

Renal 2 (12 decks)

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