Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Prerenal azotemia

A

Results from hypoperfusion of the kidneys

Impairs renal function in absence of parenchymal damage

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

Postrenal azotemia

A

Urine flow is obstructed distal to the kidney

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

Uremia

A

Azotemia + other signs/symptoms/abnormalities

Failed excretory function + metabolic and endocrine alterations

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

Common systems effected by uremia

A

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

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

Nephritic syndrome

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

Ex. acute poststreptococcal glomerulonephritis

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

Rapidly progressive glomerulonephritis

A

Rapidly declining GFR (hours to days)

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

Nephrotic syndrome

A 
Glomerular disease
**Proteinuria (greater than 3.5 gm/day)
Hypoalbuminemia
Edema
Hyperlipidemia and lipiduria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Asymptomatic hematuria or proteinuria

A

Mild glomerular abnormalities

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

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

ESRD

A

GFR less than 5%

Terminal uremia

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

Renal tubular defects

A

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

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

Renal tumors and urinary tract obstruction

A

Depends on location and nature of lesion

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

UTI

A

Bacteruria and pyuria

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

Nephrolithiasis

A

Spasms of severe pain and hematuria

High recurrence

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

Most common cause of CKD

A

Diabetes and HTN

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

Major cause of death from renal disease

A

CKD

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

Tracking CKD

A

Creatinine levels

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

Systemic manifestations of uremia and CKD

A

Table 20-1

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

Secondary glomerular diseases

A

Systemic disease injuring glomeruli

SLE, HTN, DM, amyloidosis, Fabry disease

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

Primary glomerularnephritis

A

Only kidney involved

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

Glomerulopathy

A

No inflammatory component

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

General Glomerulus structure

A

Capillary network

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
GBM
Lamina densa - thick central layer Lamina rara externa and interna - thin peripheral layers Type IV collagen
26
Proteoglycan content of GBM
Permeability characteristics
27
NC1 domain of GBM
Important for collagen structure | Target for antibodies
28
Alpha-chains of GBM
Underlie some forms of hereditary nephritis
29
Podocytes
Interdigitate and are separated by filtration slits bridged by thin diaphragm
30
Mesangial cells
``` Supporting cells (can contract, proliferate and secrete necessary material) Form matrix surrounding capillary ```
31
Glomerulus permeability
Highly permeable to water and small solutes Impermeable to proteins (depending on charge and size) Visceral layer - size restriction
32
Exclusion of albumin
Charge dependent restriction of anion
33
Nephrin
Bridges filtration slit Anchored by CD2 attached to actin Defects can lead to defects in permeability
34
Hypercellularity
Inflammatory diseases increase number of cells in glomerular tufts Caused by: Proliferation of mesangial or endothelial Leukocyte infiltration
35
Endocapillary proliferation
Swelling of cells and infiltration of leukocytes
36
Formation of crescents
Accumulations of cells (including epithelial proliferation) with deposition of fibrin Follows immune/inflammatory injury to capillary walls
37
Basement membrane thickening
Deposition of increasingly dense material Increased synthesis of proteins Adding additional layers
38
Hyalinosis
Accumulation of material that is homogenous and eosinophilic May obliterate capillary lumens Result of endothelial or capillary wall injury
39
Sclerosis
Deposition of extracellular collagenous matrix *Diabetic glomerulosclerosis May obliterate capillary lumens
40
Chronic glomerular injury response
BM thickening, hyalinosis and sclerosis
41
Acute glomerular injury response
Hypercellularity | Severe injury - formation of crescents
42
Immune mechanisms
Most forms of primary glomerulopathy and many forms of secondary glomerular disorders
43
Two forms of antibody related injury
1) Antibodies reacting directly to glomerulus 2) Antigen-antibody complexes from circulation depositing in glomerulus **Major cause - in situ complex formation
44
In situ formation of immune complexes
Antibodies react with intrinsic tissue or extrinsic antigens "planted" in the glomerulus from circulation
45
Granular immune deposition
Very localized antigen-antibody interaction | **Most cases
46
Primary membranous nephropathy
Autoantibodies to endogenous material in tissue
47
Secondary membranous nephropathy
Drug induced Graft-versus-host disease Possible uncontrolled B cell activation
48
Linear immune deposition
Classic anti-GBM disease
49
Planted antigens
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
Anti-GBM disease
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
Circulating immune complexes
No specificity for glomerulus Physiochemical properties and hemodynamics of glomerulus bring them there Exogenous or endogenous antigens **In situ formation still more probable
52
Microbial antigens leading to glomerulonephritis
``` Bacterial products (strep) SA of Hep B SA of Hep C Treponema pallidum, plasmodium falciparum and several others Tumor ```
53
Cationic antigens
Cross GBM | Complexes reside subepithelially
54
Anionic antigens
Don't cross GBM | Subendothelial or not nephrogenic
55
Neutral antigens
Tend to accumulate in mesangium
56
Large complexes
Not as nephritogenic
57
Pattern of localization influenced by
Charge, size, hemodynamics, mesangial function, charge barrier integrity
58
Subepithelial
Less likely to involve inflammatory processes Acute glomerulonephritis
59
Epimembranous deposits
Membranous nephropathy | Heymann nephritis
60
Subendothelial deposits
More likely to involve inflammatory processes Lupus nephritis Membranoproliferative glomerulonephritis
61
Mesangial deposits
IgA nephropathy
62
Cell-Mediated immunity and glomerulonephritis
Sensitized T cells can propagate inflammatory response
63
Alternative complement pathway activation
Dense-deposit disease or membranoproliferative glomerulonephitis (MPGN Type II) or C3 glomerulopathies
64
Neutrophils and monocytes
Result from complement activation (5a) and Fc activation | GBM degradation, ROS damage cells, arachidonic acid metabolites reduce GFR
65
Macrophages and T cells
Release biologically active molecules
66
Platelets
Vascular injury and proliferation of glomerular cells
67
Resident cells
**Mesangial cells Produce inflammatory mediators Even in absence if leukocytic infiltration
68
Complement activation
Induce leukocyte influx MAC complex: cell lysis and stimulate mesangial cells **Can produce proteinuria without neutrophils
69
Hemodynamic changes
Eicosanoids, NO, angiotensin, endothelin
70
IL-1 and TNF
Produced by infiltrating leukocytes and resident cells | Leukocyte adhesion and other effects
71
Growth factors
Mesangial proliferation and hyalinization
72
VEGF
Maintain endothelial integrity and may help regulate capillary permeability
73
Coagulation system
Deposition of fibrin | Crescent formation
74
Podocytopathy
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)

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