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Renal Physiology > Glomerular Structure & Mechanisms of Disease - Nichols > Flashcards

Glomerular Structure & Mechanisms of Disease - Nichols Flashcards

1
Q

t or f: the urinary space within the glomerulus is not continuous with the urinary space in the renal tubule originating from it.

A

false. it is continuous

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2
Q

am i hungover and are these words making sense

A

yes and no…fuck

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3
Q

what covers the capillaries of the glomerular tuft?

A

podocytes (cells with feet) and their foot processes (pediceles)

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4
Q

what supports the glomerular tuft?

A

the mesangium

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5
Q

what are mesangial cells?

A

mesenchymal cells that are the equivalent of pericytes in other capillary territories.

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6
Q

are there a lot of places that glomerular disease can occur and do we classify them based on where they occur?

A

yes yes

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7
Q

explain the difference between a primary and secondary glomerular disease

A

primary are disease that occur only or predominantly in the glomerulus

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8
Q

what are various examples of primary glomerular disesase

A 
minimal change disease
focal segmental glomerulosclerosis
membranous nephropathy
acute post-strep glomeruloneph
membranoproliferative glomerulonephritis
iga nephropathy (berger disease)
hereditary nephritis (alport syndrome
congential nephrotic syndrome
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9
Q

what are some exmaples of secondary glomerular diseaes

A 
htn nephropathy
diabetic nephropathy
lupus nephritis
amyloidosis
goodpasture syndrome
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10
Q

what percentage of glomerular diseaes in children in primary? adults?

A

95%

60%

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11
Q

what is the most common glomerular disease?

A

hypertensive nephropathy

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12
Q

what is the scond most common glomerular disease?

A

diabetes mellitus

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13
Q

explain how hydrostatic pressure drives filtration in the glomerulus

A

glomerular capillaries have a higher pressure (50) than other capillaries and higher than the bowmans space (18). then yea… it works

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14
Q

what can supra-normal glomerular capillary pressure cause?

A

it stimulates gbm thickening and mesangial cell hypertrophy and hyperplasia and mesangial matrix production.

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15
Q

what can supra-normal pressure cause in the afferent arterioles?

A

high bp causes hyaline sclerosis of the afferent arterioles of glomeruli, but NOT of the efferent arterioles.

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16
Q

what can cause hyaline sclerosis of afferent AND efferent arterioles?

A

diabets mellitus

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17
Q

explain the mechanism of hyaline sclerosis in both diabetes mellitus and high blood pressure

A

plasma leaks into the wall and gradually narrows the lumen. the narrowing of the afferent arteriole is followed by gradual ischemic atrophy of the glomerulus

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18
Q

what is arterionephrosclerosis?

A

it’s a global sclerosis of the glomeruli due to the hyaline deposition and narrowing of the lumen of the afferent arteriole.

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19
Q

which population has a high rate of end-stage renal failure due to hypertension?

A

blacks

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20
Q

explain the most-likely bullshit genomic mutation from nichols that may (but doesn’t) explain why blacks have a high rate of renal failure.

A

a mutation in the gene for apolipoprotein L1, which confers resistance to african sleeping sickness due to trypanosoma brucei rhodesiense. and it’s racist to assume all black people are from africa…

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21
Q

what is the difference between hypertensive nephropathy and malignant hypertensive nephropathy?

A

the malignant form progressives very rapidly, is a multi-organ syndrom, is more common in black males age 40.

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22
Q

what are the symptoms and signs of malignant hypertensive nephropathy?

A

headache, scotomas, vomiting. bp about 200/120. proteinuira hematuria.

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23
Q

what is the classic appearance of a histological slide showing a person with malignant hypertensive nephropathy?

A

onion-skin appearance of the glomeruli

24
Q

what three diseases have hyperplastic arteriosclerosis and arterial fibrinoid necrosis?

A

malignant hypertensive nephropathy, thrombotic microangiopathies, scleroderma renal crisis.

25
Q

what causes the flea-bitten look of the kidney in malignant hypertension?

A

small arterioles and arteries can rupture all over the kidney.

26
Q

what is the most common cause of glomerular disease?

A

HTN, partly becasue glomerular disesase causes HTN, creating a positive feedback loop

27
Q

as much as 50% of the capillary endothelial surface of the glomerular capillaries have what?

A

fenestrations (windows)

28
Q

what does the lack of a continuous cytoplasmic barrier facilitate?

A

filtration and accessibility of macromculs (including Abs) to the glomerular basement membrane

29
Q

how is the glomerular basement membrane a trilaminar structure?

A

it consists of a lamina lucida interna, lamina densa, and lamina rara externa

30
Q

what are the major components of basements membranes?

A

perlecan, entactin, fibronectin, laminin, type IV collagen.

31
Q

what is the significance of the presence of perlecan in the basement membrane?

A

it’s highly charged, having heparan sulfate as the major glycosaminoglycan component. it gives most of the strong negative charge properties of basement membranes, affecting passage of proteins (which are also largely negatively charged)

32
Q

which basement membrane component has calcium binding ability?

A

entactin

33
Q

explain the shape of the collagen

A

most of the collagen is in the typical helical conformation, but there is a non-helical globular domain called the non-collagenous domain.

34
Q

why is the non-collagenous domain important?

A

there are antibodies that target the NC1 domain of alpha3 chains. This can lead to glomerulonephritis with hematuria along with pulmonary hemmorhage and hemoptysis (basically goodpastures syndrome)

35
Q

do men or women have a thicker glomerular basement membrane? who has more anti-gbm disease

A

men and men

36
Q

explain the interdigitating stuff

A

podocytes cover the capillaries with a vast network of pedicele (foot processes) that are arranged in an interlocking fashion.

37
Q

what is between the pediceles that connects them

A

slit pore diaphragm

38
Q

what is effacement?

A

fusion of foot processes, with a retraction of foot processes and a loss of slit pore diaphragm.

39
Q

what is the result of retraction of foot processes?

A

long sections of the capillaries are enveloped by a single podocyte. also, the foot processes detach from the basement membrane (due to increased pressure), causing degradation of the gbm (allowing proteins to leak from plasma into the urinary space).

40
Q

what is occurring if you see a crescent-shaped area of inflammation?

A

a proliferation of parietal epithelial cells from crescentic glomerulonephritis. this is from a leakage of plasma proteins, mixed with abs and inflammatory cytokines and ROS.

41
Q

what is the minimal space between two pediceles called?

A

the filtration slit

42
Q

what transmembrane glycoprotein is a major component of the selit pore diaphragm?

A

nephrin, which bind to each other on adjacent pediceles by disulfide linkage

43
Q

what are mesangial cells?

A

mesenchymal cells with phagocytic and contractile properties.

44
Q

what do the contractile properties of mesagnial cells do?

A

they allow the cells to regulate glomerular blood flow.

45
Q

what do the phagocytic properties of mesangial cells do?

A

scavenge substances that leakinto the mesangial matrix

46
Q

what is IgA nephropathy?

A

abnormal iga production that collects in the mesangial matrix, leading to the activation of the complement cascade leading to injurious inflammation.

47
Q

what are the three sites of immune complex deposition within glomeruli?

A

subepithelial, subendothelial and mesangail.

48
Q

in lupus, where do you see the wire loops formation?

A

subendothelial

49
Q

are immune complexes deposited linearly or granularly?

  • post-strep glomerulonephritis
  • anti-GMB
A
  • granular

- linear

50
Q

what is seen by immunofluoresence when a puerson has crescentic glomerulonephritis?

A

“pauci-immune” nothing is seen at all. lack of immune system proteins

51
Q

what causes non-enzymatic glycosylation of proteins in blood and GBM?

A

hyperglycemia

52
Q

explain the mechanism of metabolic (diabetic) glomerular injury

A

some of the glycosylated plasma proteins get trapped in the gbm, stimulating production of new gbm proteins. this leads to a thickened gbm.

53
Q

what happens when glycosylated proteins are further glycosylated?

A

they are metabolized to advanced glycation end products (age) that cause accelerated aging effects of diabetes on organs throughout the body.

54
Q

what is proliferative glomerulonephritis?

A

increased cellularity including proliferative cells native to the glomerulues, but also with infiltrating inflammatory cells.

55
Q

what is membranous glomerulopathy?

A

increased gbm without increased cells

56
Q

what is membranoproliferative disease

A

a combo of the two.

57
Q

what is glomerulonephritis described as crescentic?

A

proliferating parietal epithelial cells and infiltrating macrophages and infammatory exudate and leaked plasma creat a crescent of inflammation around the tuft of capillaries.

Renal Physiology (26 decks)

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