Brainscape's Knowledge GenomeTM

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


See full index

MHD > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

Hematuria

A

Blood in the urine
Can by glomerular (nephrologic), hallmark of nephritic syndrome
Or extraglomerular (urologic)

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

Nephritic Syndrome

A

Clinical entity, usually acute onset

  • Hematuria w/ dysmorphic cells and RBC casts
  • Some degree of oliguria and azotemia
  • Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute Postinfectious Glomerulonephritis

A

Children: Acute Nephritic Syndrome (hematuria, edema, HTN, renal failure)
Adults: Acute Nephritic Syndrome may be less common

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

Acute Postinfectious Glomerulonephritis

Epidemiology

A

Typically in children 6-10 years
Rarer in adults
Sporadic or endemic

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

Acute Postinfectious Glomerulonephritis

Etiology

A

1-4 weeks after recovery from infection
Pharynx Group A-B-hemolytic Streptococcal infections (GABHS), nephritogenic, M protein virulence factor
Other infections (pneumo, staph, viral)
Skin (impetigo)

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

Acute Postinfectious Glomerulonephritis

Pathogenesis

A

Immune complexes form in circulation (antigen + igG)
Deposition of immune complexes in capillary wall of glomerulus
Complement is activated (C5a)
Neutrophils attracted, mediate damage
Endocapillary proliferation and structural damage
“Swiss cheese” appearance with hematuria
Immune complexes are also formed IN-SITU (SUBEPITHELIAL DEPOSITS OR HUMPS) Unique to this syndrome

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

Acute Postinfectious Glomerulonephritis

Histology

A 
Endocapillary proliferation (hypercellular tuft, capillaries occluded)
neutrophilic infiltration (tri-lobed cells)
Immune complex deposits by immunofluorescence and electron microscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute Postinfectious Glomerulonephritis

Laboratory Tests

A 
Tea-colored (smokey/coca cola) urine
Hematuria, mild proteinuria
ASO titer INC
Complement levels DEC
Biopsy only required if course is ATYPICAL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute Postinfectious Glomerulonephritis

Prognosis

A

Children TOTAL RECOVERY in >95%
Adults have slow progression to chronic glomerulonephritis (because not identified until they go into renal failure)
15-50% of adults develop ESRD
Small subset of children/adults may develop severe acute illness

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

Acute Postinfectious Glomerulonephritis

Treatment

A

Supportive

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

IgA Nephropathy (Berger Disease)

A

RECURRENT gross and microscopic hematuria
Episodes of gross hematuria w/in 1-2 days of nonspecific URI (or GI or UTI)
Painless hematuria following infection
Hematuria for days, recurrence every few months
Henoch-Schoenlein purpura (main in children, small vessel vasculitis, purpura on skin, GI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
IgA Nephropathy (Berger Disease)
Epidemiology
A

IgA nephropathy = most common glomerular disease worldwide

In children and young adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
IgA Nephropathy (Berger Disease)
Etiology
A

Mucosal (respiratory, GI from food/bacteria) infection leads to IgA production
IgA immune complexes form and deposit in mesangium
Genetic or acquired abnormality in immune regulation
Abnormality in clearance of IgA
Antibodies against abnormally glycoslyated IgA
Activation of complement via alternative (rather than classic) pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q 
IgA Nephropathy (Berger Disease)
Histology
A

Mesangial proliferation (big spots on immunofluorescence)
IgA-complex in mesangium
Electron dense deposits by electron microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
IgA Nephropathy (Berger Disease)
Laboratory Tests
A

Hematuria
Mild proteinuria
Complement levels NORMAL (liver is able to keep up with complement consumption)
Usually need biopsy for diagnosis/prognosis (see how much glomerulus is involved)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q 
IgA Nephropathy (Berger Disease)
Prognosis
A

Variable -> dependent on glomerular pathology
If prolonged can lead to renal failure
Small proportion of patients get aggressive course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q 
IgA Nephropathy (Berger Disease)
Treatment
A

Supportive

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

Hereditary Nephritis

A

Group of inherited glomerular diseases
MUTATIONS in glomerular basement membrane proteins
Structural alteration, error in synthesis of IV collagen (kidney, lens, cochlea)
Alport Syndrome
- nephritis
- nerve deafness
-various eye disorders, early cataracts

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

Hereditary Nephritis

Typical Clinical Presentation

A

Hearing and ocular abnormalities

Isolated hematuria

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

Hereditary Nephritis

Epidemiology

A

Age 5-20 at presentation

20-50 years with overt renal failure

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

Hereditary Nephritis

Etiology

A

X-linked inheritance
(+) family history
Male pts: full spectrum
Female pts: carries, rare with disease (X-chromosome inactivation)

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

Hereditary Nephritis

Pathology

A

Lamina dense splitting and lamination
“Basket weave”
Is not 3 distanct layers anymore

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

Hereditary Nephritis

Histology

A

Normal in parrafin sections
NO IMMUNE COMPLEX ( - immunofluoroscopy)
Electron microscopy is diagnostic (basket weave)

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

Hereditary Nephritis

Laboratory tests

A

Hematuria

Genetic Testing

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

Hereditary Nephritis

Prognosis

A

Overt renal failure between 20-50 years of age

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

Hereditary Nephritis

Treatment

A

Supportive
Transplantation
Counseling
Family Testing (prenatal testing is available)

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

Rapidly progressive glomerulonephritis (RPGN)

A

Rapidly progressive loss of renal function
Nephritis syndrome, gross hematuria
Cresents

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

Glomerular cresent

A 
Glomerulus turns into a cresent shape
Stops bleeding but compressed tuft
Decreases filtration
Rapid progression to renal failure
If there is severe glomerular basement membrane injury, blood and FIBRIN and MACROPHAGES leak into Bowman space, parietal epithelial cells proliferate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of cresents

A

Anti-glomerular basement antibody (RPGN type I)
Some circulating immune complex glomerulonephritis (RPGN type II)
Pauci-immune/ANCA associated (RPGN type III)

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

Rapidly progressive glomerulonephritis (RPGN) Type I

A

Gross hematuria
Drop in urinary output (acute renal failure)
Hemoptysis (small capillaries in lung are involved as well)
KIDNEY AND LUNG

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

Rapidly progressive glomerulonephritis (RPGN) Type I

Epidemiology

A

Young men
Rare
12% of cresentic glomerulonephritis

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

Rapidly progressive glomerulonephritis (RPGN) Type I

Etiology

A

Anti-glomerular basement membrane antibodies
Exposure of basement membrane: viruses, smoking, solvents (paints, dyes), drugs, industrial exposure
Genetic predisposition to autoimmunity

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

Rapidly progressive glomerulonephritis (RPGN) Type I

Histology

A

Immunofluorescence: Antibody deposited along entire length of glomerular basement membrane
Membrane destroyed, multiple areas of necrosis (GROSS HEMATURIA)

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

Goodpasture Syndrome

A

Antibody cross-reactivity with pulmonary alveolar basement membrane
Linear IgG deposits along glomerular and alveolar basement membranes
Antigen: noncollagenous protein (NC1)
Rapidly progressive glomerulonephritis and hematuria and pulmonary hemorrhage (hemoptysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Rapidly progressive glomerulonephritis (RPGN) Type I

Pathology

A

Crescents
Linear stain for IgG (not seen by electron microscopy)
IgG in glomeruli/pulmonary alveoli

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

Rapidly progressive glomerulonephritis (RPGN) Type I

Laboratory tests

A

Anti-glomerular basement membrane antibodies in serum

Levels may be low in rapid binding on kidney

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

Rapidly progressive glomerulonephritis (RPGN) Type I

Prognosis

A

Renal failure

Pulmonary failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Rapidly progressive glomerulonephritis (RPGN) Type I

Treatment

A

Plasmapharesis

Removal of pathogenic antibodies from the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Clinical Presentation

A

Gross hematuria

Drop in urinary output (acute renal failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Epidemiology

A

Rare
1% of postinfectious, small subset of IgA
Systemic lupus erythematosus (SLE)
Children, young adults (10-40 yo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Etiology

A

Severe immune complex formation with necrosis

Breaks in glomerular basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Pathology

A

Crescents
Immune complexes (IgG+C3; IgA+C3)
Electron dense deposits by electron microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Laboratory tests

A

Depends on etiology (ie postinfectious, IgA nephropathy, diffuse proliferative lupus)
Postinfectious: complement drop and ASO titers
IgA: no complement drop
SLE: no complement drop
Biopsy needs to be done because presentation clinical picture is not specific enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Prognosis

A

Chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Rapidly progressive glomerulonephritis (RPGN) Type II

Treatment

A

Immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

A

ELK (eyes/ears/nose, lungs, kidneys)
Drop in urinary output (acute renal failure)
Gross hematuria
Hemoptysis, SOB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Epidemiology

A

Older patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Etiology/pathogenesis

A

Antineutrophil cytoplasmic autoantibodies (ANCA)
ANCAs react w/neutrophils causing early degranulation and release of lytic enzymes
ANCAs are present in serum
DO NOT form circulating immune complexes
Direct cause of pauci-immune crescentic glomerulonephritis/systemic vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Laboratory Tests

A

Immunofluorescence on neutrophils: the ANCA shows up

ANCA: test for their presence

50
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Pathology

A

Crescents
Extraglomerular vasculitis
NO immune complex deposits
NO electron dense deposity
NO anti-glomerular basement membrane autoantibodies
Immunofluorescence: negative (pauci immune)
Electron microscopy: negative (pauci immune)
In routine studies we don’t see the offending body, because there are no complexes deposited in kidney

51
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Prognosis

A

Renal failure

Pulmonary

52
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Treatment

A

Immunosuppression

53
Q

Rapidly progressive glomerulonephritis (RPGN) Type III

Wegener granulomatosis

A

Vasculitis with necrosis and granuloma-like pathology
c-ANCA
Ear/nose/throat
Lung
Kidney
(remember Goodpasture is just lung/kidney)

54
Q

Churg-Strauss Snydrome

A 
Allergic granulomatosis and angiitis
Small vessel necrotizing vasculitis with eosinophils
Asthma, alleric rhinitis
Lung infiltrates
Peripheral eosinophilia
Extravascular necrotizing granulomas
Palpable purpura
GI bleeding
Renal disease
myocardial infiltrates
p-ANCA
55
Q

Recap:

Type I RPGN

A

Anti glomerular basement membrane autoantibodies
Children
Goodpasture
Antibody against collagen in glomerular and alveolar basement membrane
Hematuria + hemoptysis
Young adult male

56
Q

Recap:

Type II RPGN

A 
Circulating immune complex
Young adults
Post-strep, diffuse proliferative glomerulonephritis
Diffuse immune complex deposition
Usually subendothelial
Most common in lupus
57
Q

Recap:

Type III RPGN

A 
Pauci immune/ANCA
Elderly
Wegener granulomatosis (c-ANCA)
Microscopic angiitis (p-ANCA)
Churg-Strauss (p-ANCA)
Eosinophils and asthma in Churg-Strauss
58
Q

Nephrotic Syndrome

A

Increased permeability to plasma proteins
Membrane becomes more porous to proteins (not RBCs)
Massive proteinuria > 3.5 g daily
Hypoalbuminemia

59
Q

Membranous Nephropathy

Clinical Presentation

A

Edema (looks like CHF in elderly)
Thrombosis (loss of ATIII)
Infections
10% in SLE pts

60
Q

Membranous Nephropathy

Epidemiology

A

Young/middle age adults between 30 and 60
30% adults, second most common nephrotic syndrome
5% in children
85% autoimmune (idiopathic), 15% secondary

61
Q

Membranous Nephropathy

Etiology

A

In-situ subepithelial immune complex formation
Autoimmune response against renal antigen
Carcinomas (lung, colon, breast, kidney), leukemia, non-Hodgkin’s lymphoma
Infections: malaria, hep B and C, congenital syphilis, leprosy
Drugs: penicillamine, gold

62
Q

Membranous Nephropathy

Pathogenesis

A 
In-situ immune complex formation
Antibody against glomerular antigens
IgG + complement granular deposits
Rxn on basal surface of podocytes
Injury to podocytes, loss of slit diaphragms
Foot process effacement
NO cellular rxn (no proliferation/WBCs)
NO INFLAMMATORY RESPONSE
63
Q

Membranous Nephropathy

Histology

A

No inflammation, no proliferation
Electron microscopy: subepithelial deposits
Immunofluorescence: granular deposits of IgG and C3
Silver stain: spike and dome (immune complex deposits are silver negative, basement membrane is black)
Capillary wall looks thickened and stiffer

64
Q

Membranous Nephropathy

Laboratory Tests

A

Nephrotic snydrome (hypoalmbuminemia, hyperlipidemia, lipiduria)
Secondary hyperlimidemia, inc in total cholesterol
Inc in LDL, cholesterol
Accelerated atherogenesis
NO COMPLEMENT DROP (bc chronic and slowly progressing)
Antibody testing for PLA2R
NEED TO BIOPSY, clinical presentation is too vague

65
Q

Membranous Nephropathy

Prognosis

A

1/3 pts will have spontaneous remission
1/3 progress to require dialysis
1/3 continue to have proteinuria, without progression to renal failure

66
Q

Membranous Nephropathy

Treatment

A 
Difficult
Immunosuppressive drugs (Prednisone)
Non-specific anti-proteinuric
Secondary: Tx of underlying disease
Recurrence after transplantation
67
Q

Minimal Change Disease

Clinical Presentation

A

Edema (periorbital, generalized)

68
Q

Minimal Change Disease

Epidemiology

A

Children 2-6 yo
65% of nephrotic syndrome in children
NO BIOPSY IF UNCOMPLICATED in course
Adults, 10% nephrotic syndrome in adults, need biopsy

69
Q

Minimal Change Disease

Etiology

A

REVERSIBLE podocytes injury
T cell derived, ?cytokines
Dpression of immunity (viral infections, Hodkin disease)
NSAIDs

70
Q

Minimal Change Disease

Pathology

A 
No inflammation/cellular proliferation
No immune complex deposits
Effacement (fusion) of foot processes
Membrane becomes thicker but more permeable
Reversible (with steroids
71
Q

Minimal Change Disease

Histology

A

Normal paraffin sections
No immune complex deposits
Foot processes effacement via electron microscopy

72
Q

Minimal Change Disease

Laboratory Tests

A

Nephrotic Syndrome

73
Q

Minimal Change Disease

Prognosis

A

Several episodes of nephrotic syndrome (relapses)
Normal renal function
Resolution at puberty

74
Q

Minimal Change Disease

Treatment

A

Steroids

75
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Clinical Presentation

A 
Nephrotic syndrome
Higher incidence of hematuria
Reduced GFR
HTN
Non-selective proteinuria (albumin only)
76
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Epidemiology

A

Adults 35%, most frequent pathology in human biopsy
Children 10%, older children
African American
Hispanic

77
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Etiology

A

IRREVERSIBLE injury to podocytes

78
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Histology

A

Some normal glomeruli
Some focal (segmental) obliteration (sclerosis) of glomerular capillaries
Collapse of capillary loops, increase in mesangial matrix
Immunofluorescence: negative
Electron microscopy: effacement of epithelial foot processes in ALL GLOMERULI

79
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Progression

A 
Initially only rare glomeruli involved (focal)
Preferentially juxtamedullary glomeruli
With progression more glomeruli involved
Global sclerosis
Tubular atrophy, interstitial fibrosis
80
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Pathology

A

Segmental obliteration (sclerosis) of capillaries
Collapse of capillary loops
Inc. mesangial matrix
Initially only rare glomeruli involved (focal)

81
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Laboratory Tests

A

Nephtrotic syndrome

Genetic testing

82
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Prognosis

A

Progression to renal failure

83
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Treatment

A

Initially steroid responsive
Progressively steroid dependent/resistant
Recurrence in transplants

84
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

Genetics

A

Inherited mutations in genes encoding slit diaphragm proteins
Genetic risk allels in APL1 in AA, adult-onset
Can be diagnosed in very young childnren

85
Q

Focal and Segmental Glomerular Sclerosis (FSGS)

HIV varient

A

Collapse of tuft + proliferation of visceral epithelial cells
Normally podocytes cannot proliferate
HIV induces dedifferentiation, restores their ability to proliferate
Progression is rapid/dramatic, aggressive form
Morphology looks different
Wrinkled/collapsed

86
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Clinical Presentation
A

Nephrotic syndrome and hematuria

87
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Epidemiology
A 
Older children (10%)
Adults (10%)
88
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Etiology
A

Immune complex formation
Classical complex activation
Secondary: chronic autoimmune disorders, hepatitis, endocarditis, chronic bacterial infections
Monoclonal proteins (aka paraproteins) produced by clonal B cells/plasma

89
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Pathology
A

Thicken glomerular basement membrane
“Double contour”or “tram track” on silver stain
IgG + complement deposits, subendothelial
Increase in mesangial cells (chase immune complexes into walls)
Lobular tufts
Thicke glomerular basement

90
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Laboratory Tests
A

Low complement

91
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Prognosis
A

Progression to renal failure

92
Q 
Membranoproliferative Glomerulonephritis (MPGN)
Treatment
A

Treat underlying disease (endocarditis, hepatitis, etc)

93
Q

Dense Deposit Disease

Clinical Presentation

A

Nephrotic syndrome with hematuria

94
Q

Dense Deposit Disease

Epidemiology

A

Rare

Older children

95
Q

Dense Deposit Disease

Etiology

A

Sustained activation of complement via alternative pathway (non-antibody mediated)
No antigen-antibody formation

96
Q

Dense Deposit Disease

Pathology

A

Complement (C3)
C3 convertase is usually digested quickly, but if something that prevents its removal the cascade keeps going
No immunoglobulin
Dense deposits within lamina densa (seen via electron microscopy)

97
Q

Dense Deposit Disease

Laboratory Tests

A

Complement levels

Molecular studies

98
Q

Dense Deposit Disease

Prognosis

A

Poor
Progression to renal failure
Recurrence in transplants

99
Q

Dense Deposit Disease

Treatment

A

New therapies controlling complement activation

100
Q

Diabetic nephropathy

A

Glomerular lesions
Diffuse and nodular glomerular sclerosis + nephritic syndrome
Atherosclerosis and arteriosclerosis
Pyelonephritis (acute & chronic)
Nonenzymatic glycosylation of vascular basement membrane resulting in hyaline arteriosclerosis

101
Q

Amyloidoses

A 
Deposits of anormally folded protein
Congo red positive
Plasma cell dyscrasia/multiple myeloma
Kidney involvement: nephrotic syndrome
FAT biopsy for screening!
Tx depends on protein type
Survival improves with early diagnsis
102
Q

SLE

A

Systemic lupus erythematosus
Multisystem, renal involvement with edema
Primarily young women
Immune DNA-antiDNA complexes
Proliferative glomerulonephritis with necrosis and cresents
Nephritic syndrome
10% develop nephrotic syndrome
Do kidney biopsy for staging
Tests: autoantibodies, ANAs, anti-sm, anti-dsDNA

103
Q

Ischemic ATI

A

Acute Tubule Injury
BP drop
Severe trauma
Acute pancreatitis

104
Q

Toxic ATI

A 
Acute Tubule Injury
Drugs (antibiotics)
Contrast dyes
Poisons
Organic solvents
105
Q

Combine ATI

A 
Acute Tubule Injury
Ischemic + nephrotoxic
Mismatched blood transfusion/other hemolytic crises (hemoglobinuria)
Skeletal muscle injury (myoglobinuria)
Intratubular casts
Crystals
Interstitial components
106
Q

1st Degree Tubulo-interstitial Nephritis

A

Renal tubules and interstitium
Infections, acute and chronic
Drugs & toxins
Other (metabolic: urate, oxalate, hypercalcemia, neoplasm: multiple myeloma)

107
Q

2nd Degree Tubulo-interstitial Nephritis

A

Associated with other diseases
Glomerulonephritis
Autoimmune

108
Q

Acute Pyelonephritis

A

Bacterial infection (E. coli, proteus, klebsiella, enterobacter, streptococcus faecalis)
Also fungi and viruses
Can come via blood (hematogenous)
Or ASCENDING up the ureters

109
Q

Acute- Drug Induced Interstitial Nephritis

A

Not Dose related
IgE mediate
+ skin test to drug hapten
Delayed hypersensitivity rxn (type IV)

110
Q

NSAIDs Nephritis

A

Acute hypersensitivity interstitial nephritis
Nephrotic syndrome + renal failure
Looks like minimal change disease (foot processes effacement)
BUT WE START SEEING CREATINE IN URINE
Renal failure

111
Q

Pronephros

A

4th week

112
Q

Mesonephros

A

Caudally
Tubules degenerate
Duct persists
Mesonephric duct comes in contact with cloaca, grows cranially as ureteric bud

113
Q

Renal Dysplasia

A

Aberrant nephronic differentiation
NOT NEOPLASIA
Presence of immature elements: undifferentiated mesenchyme, cartilage
Grossly enlarged kidneys, irregular shape (bunch of grapes)

114
Q

Potter’s Sydrome

A

Fetal urine production is important for amniotic fluid development
Without amniotic fluid lungs develop poorly
Small, deformed, hypoplastic lungs

115
Q

Autosomal Recessive Polycystic Kidney Disease (ARPKD)

A 
Rare
PKHD1 gene
Enlarged kidneys
Sponge-like appearance
Dilated/elongated tubules
Liver has cysts as well, fibrosis
116
Q

Adult Polycystic Kidney Disease

A 
Pain, colic, mass, hemorrhage, hematuria, renal failure, HTN
Common
Autosomal DOMINANT
Cysts in kidney and liver
Tx is transplantation
Intracranial berry aneurysms
Mitral valve prolapse
117
Q

Aquired Cystic Disease

A

Dialysis associated
Cortical and medullary cysts
Renal cell carcinoma can occur

118
Q

Benign Kidney Tumors

A

Oncocytoma (distal nephron, mahogeny brown with central scar)
Angiomyolipoma (vessels/smooth muscle/fat, huge/irregular vessels

119
Q

Renal Cell Carcinoma

A

TRIAD: COSTO-VERTEBRAL PAIN, MASS, HEMATURIA
Incidentally discovered
Cause paraneoplastic syndromes (often how its discovered)
Found in the elderly
Very deadly
Can be sporadic or genetic
Kinda looks like adrenal gland
Extremely chemo-resistant, there are targeted therapies

120
Q

von Hippel-Lindau (VHL) syndrome

A 
Sutosomal dominant
37 years
Multiple bilateral cysts and tumors, high vascularity
Angiomas of retina
Hemangioblastoma (CNS/cerebellum/spine)
Pheos in some
121
Q

Urothelial Carcinoma

A

Adults
Renal pelvis, ureter, frequently with bladder cancer
Hematuria
ANALGESIC NEPHROPATHY is a risk factor

122
Q

Wilm’s tumor

A

25% have other developmental abnormalities
WAGR: Wilms tumor, Aniridia, Gu malformation, mental Retardation
Peds, most common kidney tumor
Malginant blastema (small blue cells, undifferentiated), tubules, stroma
Soft tumors, need to be careful when removing
Good prognosis
Very chemosensitive

MHD (34 decks)

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