Glomerular Disease: Pathogenesis of the injury, not specific diseases Flashcards Preview

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Flashcards in Glomerular Disease: Pathogenesis of the injury, not specific diseases Deck (21)
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1

Working inside to outside, what are the 4 layers of the glomerular capillary wall?

Fenestrated endothelial layer, glomerular basement membrane, visceral epithelium with foot processes and parietal epithelium surrounds the whole capsule.

2

What do we find in the middle of all the capillaries?

Mesangial matrix with mesangial cells inside

3

What does the size and charge depended barrier function mean when it comes to filtering through the glomerulus?

It means the larger something is the less permeable and the more cationic it is the more permeable.

4

What is between the visceral epithelium and the parietal epithelium?

This is the urinary space where the filtrate initially collects.

5

What are two important functions of the visceral epithelium?

It contains the slit diaphragm for selective passage and synthesis of the basement membrane components

6

What are the 4 pathologic responses of the glomerulus to injury?

Hypercellularity: proliferation of current cells or infiltration of others
Basement membrane thickening: appears as thickening of the cap wall
Hyalinosis:
Sclerosis: deposition of collagen

7

Primary glomerulopathies can be broken down by the location of their damage or injury? What are these 5 categories?

Diffuse, which is all the glomeruli in the kidney.
Global which is a whole glomeruli
Focal which is part of one glomeruli
Segmental which is part of each glomeruli
And capillary or mesangial, affecting either one.

8

What type of mechanism of injury causes most forms of glomerulopathy?

Immune mechanisms

9

What is a good/simple definition for glomerulonephritis and what is the mechanism of injury most commonly?

Damage/injury to the glomeruli. Antibody-antigen complexes or just antibody mediated injury, usually with complement involved.

10

What are the two forms of antibody-mediated injury to the glomeruli and which one is more common?

Either antibodies react to components of the glomeruli itself or deposit as an antigen-antibody complex already formed somewhere else in the body. In situ is more common.

11

What are the two types of antigens that antibodies react with in In Situ formation of immune complexes?

Intrinsic antigens already there and planted antigens from somewhere else outside of the kidney

12

What is the classic example of In Situ antibody-mediated complex injury the book mentions, what is the receptor that antibodies go after, and where do the complexes deposit?

Membranous nephropathy. PLA2R. Subepithelial aspect of basement membrane.

13

The pattern of immune deposition by immunofluorescence is what pattern for in situ antibody mediated injury and why is it important to know this?

It is granular rather than linear. This is important because you can have antibodies that are completely anti GBM against a continuous comment and it is a diffuse linear pattern across the entire length of the GBM.

14

Where do anionic, cationic, and neutral complexes deposit and which ones are nephritogenic?

Anionic don’t cross the GBM so they stay subendothelial. Cationic cross and end in subepithelial. Neutral end up in the mesangium. Cationic are nephritogenic.

15

Explain which areas of deposited complexes will also include an inflammatory reaction and why?

Complexes in the mesangium and subendothelial areas will have an inflammatory reaction included because they have access to the circulation and therefore access to leukocytes. Subepithelial complexes don’t have access to the circulation.

16

Explain the term podocytopathy and why is it such a big deal?

Disease mechanisms in which the principle manifestation of injury is to the podocytes. This is a big deal because you have screwed up the slit diaphragm. These podocytes have very limited replication and repair capacity.

17

Big picture, what happens when any renal disease destroys functioning nephrons to the point that GFR is 30-50% of normal?

There is a steady rate of progression towards end stage renal disease.

18

What are the two major histological characteristics of this steady rate progression to end stage renal failure?

Focal segmental glomerulosclerosis
Tubulointerstitial fibrosis

19

What is focal segmental glomerulosclerosis and what are 5 results of it?

Progressive fibrosis of the glomeruli.
1. Reduction in renal mass
2. Protein in urine
3. Systemic hypertension
4. Glomerular hypertension
5. Glomerular hypertrophy

20

What is the correlation we need to know concerning tubulointerstitial fibrosis?

It is better correlated with a decline in renal function than glomerular injury.

21

What did the book mention that causes direct injury to and activation of tubular cells?

Protein in the urine