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Morbid Anatomy > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

The kidney has a large functional reserve and as such there is typically damage >75% before impairment

A

True

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2
Q

The glomerulus is lined by 3 things namely

A

Fenestrated endothelium
Basement membrane
Pododcytes or foot processes

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3
Q

Gaps between endothelial cells are known as

A

Fenestrae measuring 70-100nm

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4
Q

The basement membrane of the glomerulus consists mainly of

A

Type IV collagen
Heparan sulphate
Laminin
Glycoprotein
With a thickness of 250-400nm

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5
Q

The visceral epithelia of the glomerulus is

A

Poeocytes or foot processes
Embedded into the bm and separated from adjacent ones by 20-30nm filtration skits bridged by thin diaphragm (nephrin that attaches to intracellular proteins known as podocin)

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6
Q

The parietal epithelium faces the bowman’s space and is not in contact with the BM. T/f

A

T

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7
Q

The functions of the mesangial cells of the glomerulus

A

Phagocytosis
Contractility
They lie between the capillaries

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8
Q

What are the layers of the glomerular basement membrane

A

Central lamina densa
Between a lamina rara interna and externa

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9
Q

Two types of azotemia include

A

Pre renal: reduced renal blood flow leading to hypoperfusion with or without parenchyma damage

Post renal: obstruction of urine flow beyond the level of the kidneys

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10
Q

Azotemia=asymptomatic
Uremia=symptomatic
T/f

A

Obviously
Are you dumb 😒

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11
Q

Nephritic syndrome

A

A clinical syndrome that presents as

P-proteinuria (mild-moderate)
H-hematuria (grossly visible or microscopic)
A-Anasarca (less than in nephritis syndrome tho)
R- red cell casts (from breakdown of red cells)
O- oliguria
A-azotemia
H-hypertensiom

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12
Q

Nephrotic syndrome

A

A clinical syndrome in which there is increased permeability of the glomerulus and thus presents as

H- hypoalbuminemia(<3g/dl)
H- hyperlipidemia/lipiduria
O-nephrotic
P- heavy proteinuria(>3.5g/day)
E- severe edema

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13
Q

Acute kidney injury

A

Characterised by a sudden and often reversible reduction in kidney function often denoted by
Rapid decline in GFR(within hours to days)
Concurrent dysregulation of fluid/electrolyte balance
Retention of metabolic waste(azotemia)
In severe cases, oliguria or anuria is present

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14
Q

The types of AKI and their causes include

A

Pre renal- reduced blood volume as a result of dehydration from vomiting, diarrhea etc
Hemorrhage
Shock, sepsis

Intrinsic renal…due to injury of the kidney in cases of acute tubular necrosis
Drugs, toxins, glomerulonephritis, lupus nephritis

Post renal- typically due to obstruction asin urethral stricture, bladder cancer,enlargement of the prostate

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15
Q

Chronic renal failure

A

Defined as presence of diminished GFR that is persistently less than 60ml/minute/1.73m² for at least 3 months from any cause and or persistent albuminuria
End result of all chronic renal parenchymal diseases.

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16
Q

End stage renal disease

A

occurs when the Gfr is <5% of normal . Terminal stage of uremia.

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17
Q

Secondary diseases with glomerular involvement

A

DM
SLE
Goodpastures disease
Wegener’s granulomatosis
Amyloidosis
Hence schnolein purpura

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18
Q

Pathologic responses of glomerulus to injury

A

Hate- hypercellularity( epithelia, mesengial cells or leukocyte infiltration, formation of crescents)
Sucking- sclerosis
Hate- hyalinosis
boobs-basement membrane thickening

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19
Q

Pathogenesis of glomerular injury

A

Disease caused by in situ formation of immune complexes
Diseases caused by deposition of circulating immune complexes
Due to antibodies directed against normal components of the glomerular basement membrane with crossreactivity asin good pastures disease
Cell mediated immunity in glomerulonephritis

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20
Q

Diffuse is to focal as global is to?

A

Segmental

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21
Q

Complications of nephritis syndrome

A

Infections especially staphylococcal and pneumococcal diseases probably due to loss of immunoglobulin in urine
Thrombosis(anticoagulation disorders) due in part to loss of antithrombin 3 in urine
Renal vein Thrombosis
Lipid based diseases

ESRD
Death

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22
Q

The most frequent Systemic causes of nephrotic syndrome

A

Das sad
DM
Amyloidosis
SLE

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23
Q

Uniform and diffuse effacement of podocytes is seen on light microscopy in minimal change disease

A

False, only seen on electron microscopy with no immunofluorescence

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24
Q

In which type of glomerulonephritis is there selective proteinuria typically to albumin

A

Minimal change

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25
Q

Prognosis of minimal change

A

Good to corticosteroid therapy especially children >90%
However proteinuria may recur and some patients may become steroid dependent or resistant although this typically resolves by puberty

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26
Q

Most common cause of nephrotic syndrome in adults

A

Membranous nephropathy

27
Q

About membranous nephropathy

A

Chxd by diffuse thickening of glomerular capillary wall due to accumulation of deposits containing immunoglobulin along the subepithelial side of the BM

28
Q

Approximately 75% of cases of membranous nephropathy are secondary whereas the rest are primary. T/f

A

False..other way round

29
Q

Secondary causes of membranous nephropathy

A

Drugs like gold captopril gold NSAIDs
SLE,tumors, infections, AI disorders

30
Q

Morphology of m.nephropathy

A

Light microscopy- uniform and diffuse thickening of the glomerular capillary wall
Electron microscopy- Effacement of podocytes with Irregular electron dense subepithial deposits
Immunofluorescence- granular deposits of IgG and complement

31
Q

Prognosis of membranous nephropathy

A

Variable, could be spontaneous remission or renal failure within 10-15yrs
Better response to corticosteroid in children than adults
May progress to focal segmental glonerulosclerosis

32
Q

Most common cause of nephrotic syndrome in adults in the U.S

A

Focal segmental

33
Q

What is focal segmental glomerulosclerosis

A

Here, some glomeruli exhibit segmental sclerosis whereas others are normal

34
Q

FSG occurs in the following setting

A

Primary: in which there’s no identifiable cause
Associated with other conditions: HIV, heroin Scd morbid obesity
Secondary: following igA nephropathy or m.nephropathy.
Adaptive

35
Q

Although fgs is typically nephrotic, there’s a higher incidence of nephritic symptoms including

A

Haematuria
Reduced Gfr
Hypertension

36
Q

Prognosis of fgs

A

Poor response to corticosteroids
Progression to Ckd with at least 50% and ESRD in 10yrs
Negative immunofluorescence

37
Q

Membranoproliferative glomerulonephritis produces only nephritic syndrome…t/f

A

False…produces both nephrotic and nephritic

38
Q

Membranoproliferative glomerulonephritis is histologically chxd by

A

Thickening of GBM , proliferation of endothelial and mesangial cells, leukocyte infiltration and presence of deposits in mesangial and capillary wall regions

39
Q

MPG is sometimes referred to as

A

Mesangiocapillary glomerulonephritis because the proliferation typically occurs in both cells

40
Q

“GBM is Thickened and often shows a double contour or a tram track appearance caused by duplication of the BM with accentuated lobular appearance”. This is characteristic of ?

A

Membranoproliferative glomerulonephritis

41
Q

Type I membranoproliferative glomerulonephritis is chxd by

A

Presence of discrete subendothelial electron dense deposits consisting of IgG and complement.

42
Q

Type II membranoproliferative glomerulonephritis

A

Now called dense deposit disease whereby there is excessive activation of alternative complement pathway with deposition of unknown material within the Bm associated with a circulating ab named C3 nephritic factor

43
Q

Circulatory antibody associated with dense deposit disease is known as

A

C3 nephritic factor

44
Q

Prognosis of membranoproliferative glomerulonephritis

A

Treatment not proven to be effective, about half of the patients develop ESRD Within 10yrs

45
Q

Diabetic glomerulosclerosis is also known as

A

Kimmelstiel Wilson disease or nodular glomerulosclerosis

46
Q

The earliest lesion in nodular glomerulosclerosis is

A

GBM thickening followed by glomerular enlargement
It’s highly specific for diabetes

47
Q

CRAP helps you to remember that

A

Congo Red Amyloid Positive deposits mainly in mesangium and capillaries is a feature of amyloid nephropathy

48
Q

Acute proliferative gn is also known as

A

Post streptococcal or post infectious GN

49
Q

Usually follows an acute infection with group A beta hemolytic strep, most often pharyngitis( including scarlet fever). What are we talking about

A

Acute proliferative gn

50
Q

Acute proliferative gn

A

Occurs at all ages, typically in children.
Develops 1-4 weeks after a strep infection which may have already resolved
Others S.aureus, S.pneumoniae etc
In children, good prognosis
In adults, bad significant proportion leads to CRF

51
Q

Pathogenesis of acute proliferative gn

A

Strep infxn->1- 4 weeks after-> streptolysin O antigen left behind->serum antistreptolysin O antibody(ASO) formed-> ASO combines with SO ->immune complexes formed-> deposited in glomeruli->acute proliferative gn

52
Q

Nephritogenic strains of acute proliferative gn

A

Griffiths types-12, 4,1,25 and 49

53
Q

Rapidly progressive glomerulonephritis is also known as

A

Crescentic glomerulonephritis

54
Q

Clinical features at first resemble acute proliferative but instead of regressing after a week or two , they become progressively worse leading to advanced renal failure after a period of days or weeks…what are we referring to

A

Rapidly progressive

55
Q

Pathology of post infectious gn

A

Diffuse enlargement and increased cellularity of the glomeruli
Narrowing or obliteration of the Bowman’s capsular space with part of the glomerular tuft seen to have herniated into the lumen of the PT
Narrowing of glomerular capillary lumina

56
Q

Histology of post infectious gn

A

Electron microscopy: shows the presence of subepithelial humps due to deposits of electron dense material indicative of immune complex formation
IF-shows granular deposition of Ig and complements

57
Q

In which gn is there herniation of glomerular tuft into the lumen of the proximal tubule?

A

Acute proliferative

58
Q

Aetiology of crescentic glomerulonephritis

A

Most common cause is Anti neutrophil cytoplasmic antibody(ANCA) associated vasculitis. E.g microscopic polyangitis and wegener’s granulomatosis
Also patients with anti GBM antibodies develop goodpasture’s syndrome
Rarely follows a strep infxn, represents a severe end of the spectrum of acute diffuse proliferative glomerulonephritis.

59
Q

Pathology of rapidly progressive gn

A

Chxtic Histological feature-> proliferation of the parietal epithelium of Bowman’s capsule to form epithelial crescents which in time are replaced by fibrous tissue

Also proliferation of both endothelial and mesangial cells

60
Q

Histology of rapid progressive gn

A

IF shows absence of Igs in crescents but rather deposits of fibrin are present which have been shown experimentally to stimulate formation

61
Q

Chronic glomerulonephritis pathology

A

Gross
Both kidneys are uniformly shrunken in size
Thinningof cortex and medullary pyramids are also shrunken
Noteee…that the renal pelvis and calyces are not distorted.

62
Q

Flea bitten appearance of kidney is seen in

A

In cases of chronic gn complicated by malignant htn where the cotical surface of the kidney shows molting and hemorrhage

63
Q

Microscopy of Chronic gn

A

Sclerosis and complete hyalinisation of many glomeruli. Arteries show hypertensive changes

Morbid Anatomy (6 decks)

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