Pathology 1

Question 0

Lobular

Answer 0

Hyper segmentation of normal lobular architecture of tuft due to intracapillary hypercellularity or significant mesangial expansions

Question 1

Obsolescence

Answer 1

Total loss of glomerular architecture due to scarring

Question 2

Mesangiolysis

Answer 2

Dissolution or attenuation of mesangial matrix and degeneration of mesangial cells, often associated with glomerular cap aneurysms

Question 3

Mesangial interposition

Answer 3

Extension of mesangial cells in peripheral cap walls in space between endothelial cells and GBM (sub endothelial zone)

Question 4

Wire loops

Answer 4

due to large and confluent subendothelial immune deposits

Question 5

Mesangial hypercellularity

Answer 5

Three or more mesangial and/or inflammatory cells per mesangial area in section 2-3 micrometers in thickness

Question 6

Intracapillary hypercellularity

Answer 6

In both meaangium and endocapillaries

Question 7

Humps

Answer 7

Subepithelial electron dense immune type deposits with cigar or dome like appearance

Question 8

Hydropic degeneration/osmotic nephrosis

Answer 8

Fine regular cytoplasmic vacuolization of proximal tubules

Question 9

Hypokalemic change

Answer 9

Large irregular sized coarse vacuoles in cytoplasm of tubular epithelial cells, especially distal tubular cells

Question 10

What is the definition of nephrotic syndrome?

Answer 10

Insidious onset of:
Heavy proteinuria (>3.5 g/24 hrs)
Hypoalbuminemia (plasma albumin <3 g/dl)
Severe edema
Hyperlipidemia

Question 11

What is the pathophysiology of nephrotic syndrome?

Answer 11

Increased glomerular permeability to plasma proteins
Urinary loss and increased tubular catabolism of albumin
Na and water retention by kidney, decreased plasma oncotic pressure in systemic capillaries due to hypoalbuminemia
Increased hepatic synthesis of lipoproteins (also abnormal transport of lipids and decreased catabolism)

Question 12

How is the vascular component of the kidney arranged?

Answer 12

Renal artery –> segmental artery –> inter lobar artery –> arcuate artery –> inter lobular artery –> afferent arterioles
These are end arteries and arterioles

Question 13

What are the different components of the glomerulus?

Answer 13

Endothelial cells - separates blood from GBM, fenestrated
Visceral epithelial cells = podocytes
Mesangial cells
GBM
Parietal epithelial cells line bowman’s capsule

Question 14

What do podocytes do in the glomerulus?

Answer 14

Foot processes attach to GBM and separated by filtration slits bridged by slit diaphragms
Slit diaphragms have nephrin and podocin that control permeability
Why effacement causes proteinuria

Question 15

What do mesangial cells do in the glomerulus?

Answer 15

Between capillary loops and support tuft

Synthesize mesangial matrix and share features with smooth muscle (contractile) and macrophages (phagocytic)

Question 16

What does the GBM do in the glomerulus?

Answer 16

Acellular membrane of type IV collagen and heparan sulfate

Fixed negative charge - repels negatively charged proteins

Question 17

What are the different ways of classifying renal disease?

Answer 17

Clinical - major syndromes
Etiologic - but frequently unknown
Immunopathologic - based on IF findings
Morphological - mainstay, based on LM and EM patterns

Question 18

What are most primary glomerular diseases?

Answer 18

Immunologic in nature
Exogenous or endogenous antigens can form immune complexes in circulation and deposit or in situ - activates complement and leukocytes to cause injury

Question 19

What is the pathogenesis of FSGS?

Answer 19

Overall most common nephrotic syndrome in adults
Soluble circulating permeability inducing factor cases after renal transplant
Glomerular hypertension causes podocyte injury in secondary

Question 20

What is the clinical course of FSGS?

Answer 20

At least half get end stage renal disease within 10 years

Question 21

What are the causes of secondary FSGS?*

Answer 21

Familial/genetic - nephrin gene (NPHS1) causes Finnish type, podocin gene (NPHS2) causes steroid resistant
Virus - HIV associated
Drugs - heroin, anabolic steroids, lithium, pamidronate
Adaptive structural functional - reflux, sickle cell, HTN, obesity