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renal robbins > renal robbins > Flashcards

renal robbins Flashcards

simple facts, definitions

1
Q

the study of kidney diseases is facilitated by dividing them into those that affect the four basic basic morphological components,

A

glomeruli, tubules, interstitium, and blood vessels

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2
Q

most glomerular diseases are ___ mediated, whereas tubular and interstitial disorders are frequently caused by ___

A

immunologically, toxic or infectious agents

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3
Q

azotemia

A

a biochemical abnormality that refers to an elevation of blood urea nitrogen(BUN) and creatitine levels, and is related largely to a decreased glomerular filtration rate(GFR). manifestation of acute or chronic kidney injury

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4
Q

prerenal azotemia

A

when there is hypoperfusion of the kidneys(hemorrhage, hypotensive shock, voume depeltion of any cause that impairs renal function in the absence of primary renal paryenchymal damage, like CHF, liver cirrhosis)

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5
Q

postrenal azotemia

A

seen whenever urine flow is obstructed distal to the kidney. removal of obstruction corrects the azotemia

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6
Q

uremia

A

azotemia plus a constellation of clinical findings and biochemical abnormalities resulting from renal damage. secondary involvements of GI, peripheral nerves, heart(fibrinous pericarditis). table 20-1

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7
Q

nephritic syndrome(basic def)

A

due to glomerular disease, presents with either visible hematuria or microscopic hematuria with dysmorphic red cells and red cell casts on urinalysis. diminished gfr, mild to moderate proteinuria, and hypertension

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8
Q

nephrotic syndrome(basic def)

A

also due to glomerular disease, heavy proteinuria more than 3.5 g a day, hypoalbuminea, severe adema, hyperlipidemia, and lipiduria (lipid in the urine)

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9
Q

asymptomatic hematuria or proteinuria

A

another manifestation of kidney pathology

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10
Q

acute kidney injury

A

rapid decline in GFR(hours or days), most severe forms exhibit oliguria or anuria(reduced urine flow), can result from glomerular, insterstitial, vascuar, or tubular injury, dysregulation of fluid electrolyte balance and waste retention of urea and creatinine. can be reversible or progress to CKD

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11
Q

chronic kidney disease(CKD)

A

chronic renal failure, mild, clinically silent, diminshed gfr less than 60ml/minute/1.73m^2 for at least 3 months or persistend albuminuria, CKD is irreversible. end result of all chronic renal parenchymal diseases

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12
Q

end stage renal disease(ESRD)

A

GFR is less than 5 percent of normal, end stage of uremia

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13
Q

rapidly progressive glomerulonephritis

A

signs of nephritic syndrome with rapid decline in GFR. implies severe glomerular injury

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14
Q

isolated urinary abnormalities

A

glomerular hematuria and/or subnephrotic proteinuria

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15
Q

difference between primary and secondary glomerular disease

A

primary stems from the kidney itself, secondary: diabetes, sle, vasculitis, amyloidosis(table 20-2)

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16
Q

what is the most common cause of CRF/ESRD

A

diabetes. hypertension is second. also lupus

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17
Q

describe the pthwy of filtration from the capillary to the urinary space

A

fenestrated endothelium, GBM-lamina rara interna, lamina densa(electron dense), lamina rara externa, podocyte filtration slits

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18
Q

what kind of collagen is the gbm made of

A

4

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19
Q

what does goodpasture syndrome/anti-gbm ab attach to

A

noncollagenous regions of collagen type 4

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20
Q

mesangial cells

A

lie between the capillaries, embedded in mesangial matrix, they are contractile, phagocytic, and capable of proliferation, laying down matrix and collagen and secrete biologically active mediators. important in many forms of glomerulonephritis

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21
Q

what can pass through the glomerular filtration barrier

A

small and cationic. albumin is large and negatively charged

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22
Q

visceral epithelial cell

A

podocyte. slit diaphragm presents a size selective diffusion barrier to the filtration of proteins, synthesizes gbm components. slit diaphragms are inbetween foot processes. again, size elective diffusion barrier to proteins. damage to these results in proteinuria

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23
Q

what are the four basic tissue responses to injury

A

hypercellularity, basement membrane thickening, hyalinosis and sclerosis,

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24
Q

hypercellularity

A

increase in the number of cells in the glomerular tufts. results from one or more of the following: proliferation of mesangial or endothelial cells. infiltration of leukocytes, and that along with with swelling and proliferation of mesangial and/or endothelial cells, called endocapillary proliferation. formation of crescents

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25
Q

crescents formation

A

proliferation of epithelial cells, mostly parietal, infiltrating leukocytes, after immune/inflammatory injury involving capillary walls, plasma proteins leak into urinary space, fibrin deposition

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26
Q

hyalinosis

A

accumulation of homogenous, eosiniphilic material, amorphous, extracellular. usually a consequence of endothelial or capillary wall injury, and is typically the end result of various forms of glomerular damage

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27
Q

sclerosis

A

deposition of extracellular collagenous matrix. may also result in obliteration of capillary lumens in affected glomeruli.

28
Q

diffuse

A

involving all glomeruli in the kidney

29
Q

global

A

involves entirety of individual glomeruli

30
Q

focal

A

involves only a fraction of glomeruli in the kidney

31
Q

segmental

A

affecting a part of each glomerulus

32
Q

mesangial

A

affecting mesangial regions

33
Q

chronic glomerular responses to injury include

A

basement membrane thickening, hyalinosis, and sclerosis

34
Q

membranous nephropathy

A

immune complexes are formed locally by ab that react with intrinsic tissue ag. also, heymann nephritis. reacts to pla2r, which is a protein in glomerular epithelial cell membrane. complement activation and then shedding of the immune aggregates form the cell surface to form characteristic deposits of immune complexes along the subepithelila aspect of the bm. granular immunoflourescence, thickened bm on light microscapy

35
Q

what are some ag that can be planted in the gomerulus

A

cationic molecules that bind to anionic components of glomerulus, dna, other nuclear proteins

36
Q

where are heymann and pla2r membranous nephropathy complexes seen

A

subepithelial space/epimembranous space

37
Q

what immunoflourescence pattern do planted and in situ immune complex membranous nephritis have?

A

granular

38
Q

what pattern does anti gbm have

A

linear

39
Q

what other basement membranes do anti gbm abs cross react with

A

lung alveoli, kindey lesion(goodpasture syndrome

40
Q

in glomerulonephritis from deposistion of circulating immune complexes, what are examples of ag

A

endogenous; sle, iga nephropathy. exogenous: post strep, hepatitis,

41
Q

in immune mediated glomeronephritis, what is the mechanism of injury

A

local inflammation, engagement of fc receptors on leukocytes, complement

42
Q

membranoproliferative pattern

A

subendothelial

43
Q

dense deposit disease

A

membranoproliferative glomerulonephritis II(MPGN type 2). alternative complement pthway

44
Q

___ are a feature of multiple types of glomerular injury including focal and segmental gomerulosclerosis and diabetic nephropathy

A

loss of podocytes

45
Q

once any renal disease destroys functioning nephrons and reduces gfr to ___ percent normal, progression to end stage renal failure(ESRF) proceeds at a steady rate independent of the original stimulus or activity of the underlying disease

A

30 to 50

46
Q

two major hisotological characteristics of progressive renal damage are

A

FSGS and tubulointerstitial fibrosis

47
Q

fsgs

A

focal segmental glomerulosclerosis. progressive fibrosis involving portions of some glomeruli develops after many types of renal injury and leads to proteinuria and increasing functional impairment. asoc w/ compensoatory hypertoryphy, eventually leads to total glomerular sclerosis and uremia

48
Q

tubulointerstitial fibrosis

A

tubilar damage and interstitial inflammation, is a componenet of many acture and chronic glomerulonephritides

49
Q

renal function decline is best correlated with

A

tubulointersitital damage rather than glomerular injury

50
Q

nephritic syndrome

A

inflammation in the glomeruli. hematuria, red cell casts in the urine, azotemia, oliguria, and mild to moderate hypertension

51
Q

acute proliferative comerulonephritis

A

includes poststrep, postinfectious. characterized histologically by diffuse proliferation of glomerular cells associated with influx of leukocytes. typically caused by immune complexes

52
Q

poststrep glomerulonephritis

A

1 to 4 weeks after a strep infection or the skin or pharynx. assoc with overcrowding and poor hygiene. typically age 6 to 10. fomred by immune complexes containing strep ag and ab formed in situ. subpepithelial HUMP LIKE DEPOSITS. granular deposits of igg, igm, c3 in the mesangium and bm. neutrophil in lumen. enlarged glomeruli, marked hypercellularity with proliferation of endothelial and mesangial cells, leukocyte infiltration, crescent formation in severe cases

53
Q

what is the clinical for post strep glomerulonephritis

A

slide 95/96

54
Q

rpgn

A

rapidly progressing crescentic glomerulonephritis. syndrome assoc with severe glomerular injury, but does not denote a specific etiology. severe oliguria, nephritic syndrome. can lead to death from renal failure within weeks to months. The most common histological feature is crescents. proliferation of parietal epithelial, and infiltration of monocytes and macr.

55
Q

what are the three types of rpgn

A

anti gbm, immune complex deposition, pauci immune

56
Q

what is the hla haplotype assoc with goodpasture/rpgn

A

drb1`

57
Q

what is the morphology of rpgn

A

crescents, ruptures in the gbm, blood cell leaking through bm, wrinkling of glomerular bm,

58
Q

nephrotic syndrome

A

derangement in glomerular capillary walls resulting in increased permeablility to plasma proteins. manifestations: massive proteinuria, loss of 3.5 g or more, hypoalbuminemia, generalized edema, hyperlipidemia and lipiduria

59
Q

highly selective proteinuria

A

low weight proteins, like albumin

60
Q

membranous nephropathy

A

diffusie thickening of the glomerular capillary wall due to the accumulation of deposits containing ig along the subepithelial side of the basement membrane

61
Q

what are some causes of membranous nephropathy

A

drugs nsaids, malignat tumors, lung colon carcinoma, sle, infections, hla dq1

62
Q

what is the morphology of membranous nephropathy

A

uniform, diffuse thickening of the glomerular capillary wall without increase in cells. irregular spikes seen with silver stain,

63
Q

mcg

A

minimal change disease. benign, uniform and diffuse effacement of foot processes, detectable only by electron microscopy. most frequent cause of nephortic syndrome in children. between 2 to 6. increased incidence with atopic disorders, hodgkins lymphoma. fusion of foot processes. normal glomeruli + effaced foot processes =mcg. lipoid nephrosis. highly selective massive proteinuria, mostly albumin. most patients respond to corticosteroids

64
Q

fsgs

A

most common cause of nephrotic syndrome in adults in the US. hypertension, microscopic hematuria, azotemia

65
Q

what is the hallmark of fsgs

A

effacement of foot processes

66
Q

mpgn

A

pattern of immune mediated injury rather than a disease. type 1: deposition of immune complexes containing igg and complement. type 2: dense deposit disease. c3 glomerulopathy

renal robbins (4 decks)

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