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RENAL II - Path and Phys Exam 1 > Robbins Chapter 20 - The Kidney > Flashcards

Robbins Chapter 20 - The Kidney Flashcards

1
Q

Azotemia

A 
Elevation in BUN (urea in blood)
Elevation in creatinine
Decreased GFR
Both AKI and CKD
Consequence of several renal disorders as well as extrarenal disorders
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2
Q

Prerenal azotemia

A

Results from hypoperfusion of the kidneys

Impairs renal function in absence of parenchymal damage

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3
Q

Postrenal azotemia

A

Urine flow is obstructed distal to the kidney

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4
Q

Uremia

A

Azotemia + other signs/symptoms/abnormalities

Failed excretory function + metabolic and endocrine alterations

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5
Q

Common systems effected by uremia

A

GI, peripheral nerves (neuropathy,) heart (pericarditis)

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6
Q

Nephritic syndrome

A 
Glomerular disease
Hematuria (gross or microscopic)
Decreased GFR
Proteinuria
HTN

Ex. acute poststreptococcal glomerulonephritis

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7
Q

Rapidly progressive glomerulonephritis

A

Rapidly declining GFR (hours to days)

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8
Q

Nephrotic syndrome

A 
Glomerular disease
**Proteinuria (greater than 3.5 gm/day)
Hypoalbuminemia
Edema
Hyperlipidemia and lipiduria
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9
Q

Asymptomatic hematuria or proteinuria

A

Mild glomerular abnormalities

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10
Q

AKI

A 
Glomerular, interstitial, vascular or tubular injury
Rapid GFR decrease
Dysregulation of fluid and electrolytes
Retention of metabolic waste
**Could have oliguria or anuria
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11
Q

CKD

A

Any cause, glomerulonephritis one of most common
GFR less than 60mL/min/1.73m^2 for 3 mo
Persistant albuminuria
Mild - unnoticed decline in excretory function
Severe - signs of uremia

End result of all chronic renal parenchymal diseases

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12
Q

ESRD

A

GFR less than 5%

Terminal uremia

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13
Q

Renal tubular defects

A

**polyuria, nocturia, electrolyte disorders
Structural or function defect
Function defect can be inherited or acquired

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14
Q

Renal tumors and urinary tract obstruction

A

Depends on location and nature of lesion

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15
Q

UTI

A

Bacteruria and pyuria

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16
Q

Nephrolithiasis

A

Spasms of severe pain and hematuria

High recurrence

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17
Q

Most common cause of CKD

A

Diabetes and HTN

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18
Q

Major cause of death from renal disease

A

CKD

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19
Q

Tracking CKD

A

Creatinine levels

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20
Q

Systemic manifestations of uremia and CKD

A

Table 20-1

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21
Q

Secondary glomerular diseases

A

Systemic disease injuring glomeruli

SLE, HTN, DM, amyloidosis, Fabry disease

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22
Q

Primary glomerularnephritis

A

Only kidney involved

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23
Q

Glomerulopathy

A

No inflammatory component

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24
Q

General Glomerulus structure

A

Capillary network

Fenestrated endothelium, BM separating endothelium from visceral podocytes, and parietal layer lining Bowman capsule

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25
Q

GBM

A

Lamina densa - thick central layer
Lamina rara externa and interna - thin peripheral layers
Type IV collagen

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26
Q

Proteoglycan content of GBM

A

Permeability characteristics

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27
Q

NC1 domain of GBM

A

Important for collagen structure

Target for antibodies

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28
Q

Alpha-chains of GBM

A

Underlie some forms of hereditary nephritis

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29
Q

Podocytes

A

Interdigitate and are separated by filtration slits bridged by thin diaphragm

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30
Q

Mesangial cells

A 
Supporting cells (can contract, proliferate and secrete necessary material)
Form matrix surrounding capillary
31
Q

Glomerulus permeability

A

Highly permeable to water and small solutes
Impermeable to proteins (depending on charge and size)
Visceral layer - size restriction

32
Q

Exclusion of albumin

A

Charge dependent restriction of anion

33
Q

Nephrin

A

Bridges filtration slit
Anchored by CD2 attached to actin
Defects can lead to defects in permeability

34
Q

Hypercellularity

A

Inflammatory diseases increase number of cells in glomerular tufts
Caused by:
Proliferation of mesangial or endothelial
Leukocyte infiltration

35
Q

Endocapillary proliferation

A

Swelling of cells and infiltration of leukocytes

36
Q

Formation of crescents

A

Accumulations of cells (including epithelial proliferation) with deposition of fibrin
Follows immune/inflammatory injury to capillary walls

37
Q

Basement membrane thickening

A

Deposition of increasingly dense material
Increased synthesis of proteins
Adding additional layers

38
Q

Hyalinosis

A

Accumulation of material that is homogenous and eosinophilic
May obliterate capillary lumens
Result of endothelial or capillary wall injury

39
Q

Sclerosis

A

Deposition of extracellular collagenous matrix
*Diabetic glomerulosclerosis
May obliterate capillary lumens

40
Q

Chronic glomerular injury response

A

BM thickening, hyalinosis and sclerosis

41
Q

Acute glomerular injury response

A

Hypercellularity

Severe injury - formation of crescents

42
Q

Immune mechanisms

A

Most forms of primary glomerulopathy and many forms of secondary glomerular disorders

43
Q

Two forms of antibody related injury

A

1) Antibodies reacting directly to glomerulus
2) Antigen-antibody complexes from circulation depositing in glomerulus

**Major cause - in situ complex formation

44
Q

In situ formation of immune complexes

A

Antibodies react with intrinsic tissue or extrinsic antigens “planted” in the glomerulus from circulation

45
Q

Granular immune deposition

A

Very localized antigen-antibody interaction

**Most cases

46
Q

Primary membranous nephropathy

A

Autoantibodies to endogenous material in tissue

47
Q

Secondary membranous nephropathy

A

Drug induced
Graft-versus-host disease

Possible uncontrolled B cell activation

48
Q

Linear immune deposition

A

Classic anti-GBM disease

49
Q

Planted antigens

A

Antigens that have landed in the glomerulus by interacting with intrinsic components and can have antibodies react to them and injure kidney

Cations, DNA nucleosomes, bacterial products, large aggregated proteins, immune complexes, drugs

Complex deposition appears no different from intrinsic antigens

50
Q

Anti-GBM disease

A

Antibodies homogenously distribute along entire length of GBM
These antigens are fixed and cannot be mobilized
Antibodies may cross react with different tissue
Very severe
Goodpasture syndrome

51
Q

Circulating immune complexes

A

No specificity for glomerulus
Physiochemical properties and hemodynamics of glomerulus bring them there
Exogenous or endogenous antigens

**In situ formation still more probable

52
Q

Microbial antigens leading to glomerulonephritis

A 
Bacterial products (strep)
SA of Hep B
SA of Hep C
Treponema pallidum, plasmodium falciparum and several others
Tumor
53
Q

Cationic antigens

A

Cross GBM

Complexes reside subepithelially

54
Q

Anionic antigens

A

Don’t cross GBM

Subendothelial or not nephrogenic

55
Q

Neutral antigens

A

Tend to accumulate in mesangium

56
Q

Large complexes

A

Not as nephritogenic

57
Q

Pattern of localization influenced by

A

Charge, size, hemodynamics, mesangial function, charge barrier integrity

58
Q

Subepithelial

A

Less likely to involve inflammatory processes

Acute glomerulonephritis

59
Q

Epimembranous deposits

A

Membranous nephropathy

Heymann nephritis

60
Q

Subendothelial deposits

A

More likely to involve inflammatory processes

Lupus nephritis
Membranoproliferative glomerulonephritis

61
Q

Mesangial deposits

A

IgA nephropathy

62
Q

Cell-Mediated immunity and glomerulonephritis

A

Sensitized T cells can propagate inflammatory response

63
Q

Alternative complement pathway activation

A

Dense-deposit disease or membranoproliferative glomerulonephitis (MPGN Type II) or C3 glomerulopathies

64
Q

Neutrophils and monocytes

A

Result from complement activation (5a) and Fc activation

GBM degradation, ROS damage cells, arachidonic acid metabolites reduce GFR

65
Q

Macrophages and T cells

A

Release biologically active molecules

66
Q

Platelets

A

Vascular injury and proliferation of glomerular cells

67
Q

Resident cells

A

**Mesangial cells
Produce inflammatory mediators
Even in absence if leukocytic infiltration

68
Q

Complement activation

A

Induce leukocyte influx
MAC complex: cell lysis and stimulate mesangial cells
**Can produce proteinuria without neutrophils

69
Q

Hemodynamic changes

A

Eicosanoids, NO, angiotensin, endothelin

70
Q

IL-1 and TNF

A

Produced by infiltrating leukocytes and resident cells

Leukocyte adhesion and other effects

71
Q

Growth factors

A

Mesangial proliferation and hyalinization

72
Q

VEGF

A

Maintain endothelial integrity and may help regulate capillary permeability

73
Q

Coagulation system

A

Deposition of fibrin

Crescent formation

74
Q

Podocytopathy

A

Principle manifestation is injury to podocytes

Effacement, vacuolization, retraction and detachment

Key event in developing proteinuria

RENAL II - Path and Phys Exam 1 (3 decks)

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