Glomerular Pathology Flashcards

1
Q

what characterises nephrotic disease

A
  • proteinuria
  • oedema
  • high cholesterol
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2
Q

why is oedema seen in nephrotic disease

A

the increase protein in the urine reduces the oncotic pressure in the blood

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3
Q

where does the damage in the nephron occur in nephrotic disease

A

podocytes primarily but also the basement membrane

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4
Q

what are 3 primary causes of nephrotic disease

A
  • minimal change glomerulonephritis
  • FSGS
  • membranous glomerulonephritis
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5
Q

what is minimal change glomerulonephritis

A

where circulating factors damage the podocytes meaning they don’t selectively filter as well

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6
Q

what age ranges minimal change glomerulonephritis seen

A

children

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7
Q

what is FSGS

A

where circulating factors damage podocytes and cause glomerulosclerosis

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8
Q

what is glomerulosclerosis

A

where fibrosis occurs in the glomerulus

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9
Q

what age range is FSGS seen

A

adults

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10
Q

what can be used to manage minimal change glomerulonephritis

A

steroids - as these suppress the immune system

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11
Q

what is membranous glomerulonephritis

A

where immune complexes deposit into the podocytes

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12
Q

what immunoglobulins are involved in the immune complexes seen in membranous glomerulonephritis

A

IgG

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13
Q

give 2 secondary causes of nephrotic disease

A

diabetes and amyloidosis

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14
Q

true or false: steroids help in the management of FSGS

A

false

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15
Q

what is nephritic disease

A

where there is blood lost in the urine

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16
Q

what characteristics are seen in nephritic disease

A

haematuria and hypertension

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17
Q

where in the nephron is damaged in nephritic disease

A

blood vessels

18
Q

gives some causes nephritic disease

A
  • alport syndrome
  • goodpastures syndrome
  • Thin GBM
  • vasculitis
19
Q

what is alport syndrome

A

where there is abnormal type 4 collagen meaning blood can pass through the walls of the of the GBM easier

20
Q

what is the first change that occurs in diabetic nephropathy

A

hyperfiltration and increased GFR

21
Q

what is goodpasture syndrome

A

where there is an anti-GBM antibody which leads to inflammation of the glomerulus and holes punched in the GBM allowing the passage of blood

22
Q

what is IgA nephropathy

A

where IgA is deposited in the mesangia causing an immune response and inflammation of the glomerulus - this means blood can filter through

23
Q

what is IgA vasculitis

A

where there is an anti neutrophilic cytoplasmic antibody activation which causes neutrophils to break down the GBM

24
Q

what systemic effect is seen in IgA vasculitis

A

purpura

25
Q

why are proteins filtered during hyper filtration in diabetic nephropathy

A

the increased glucose is mostly reabsorbed by the SLGT 2 transporters with salt - this means less salt reaches the macula dense resulting in dilation of the afferent and constriction of the efferent arteriole - this means more blood is in the glomerulus increasing the pressure

26
Q

what happens to the basement membrane in diabetic nephropathy

A

it becomes thicker due to an increase in glomerular pressure

27
Q

what happens to the podocytes in diabetic nephropathy

A

they become injured

28
Q

what happens to the afferent and efferent arterioles in the later stages of diabetic nephropathy

A

they both undergo fibrosis, making the lumen smaller - this decreases the GFR

29
Q

what are kimmelstiel-wilson nodules

A

fibrotic nodules that appear in the glomerulus due to too much glucose

30
Q

what is the microalbuminuria stage of diabetic nephropathy

A

where the GFR decreases back to normal
the GBM thickens, the podocytes are damaged and the mesangia expands
first time you can detect protein in the urine

31
Q

what is overt proteinuria

A

where the GFR falls rapidly giving systemic hypertension (due to less salt delivery to the macula densa)

32
Q

what is given to manage diabetic nephropathy

A

ACE inhibitors
statins
change in diet and exercise

33
Q

how do ACE inhibitors help in diabetic nephropathy

A

they prevent the actions of angiotensin 2 which causes an increase in permeability to proteins, mesangia expansion and construction of the efferent arteriole

34
Q

what is hypertensive nephrosclerosis

A

where high blood pressure causes chronic kidney disease

35
Q

what other signs will a patient with hypertensive nephrosclerosis have

A

LV hypertrophy, hypertensive eye disease

36
Q

true or false: hypertensive nephrosclerosis develops rapidly

A

false - it has a slow progression

37
Q

how is renal artery stenosis different to hypertensive nephrosclerosis

A

renal artery stenosis causes the hypertension whereas the chronic kidney disease is caused by the already present hypertension in hypertensive nephrosclerosis

38
Q

what happens to the GFR in renal artery sclerosis

A

it falls rapidly

39
Q

how do acute falls in blood pressure damage the kidneys

A

damage of the endothelium causes microangiopathic haemolytic anaemia

fibrosis of the efferent arteriole leads to necrosis and RAAS activation

40
Q

which arteriole undergoes fibrosis in hypertensive nephropathy

A

efferent arteriole