Glomerular Pathology Flashcards

(40 cards)

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

25
why are proteins filtered during hyper filtration in diabetic nephropathy
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
what happens to the basement membrane in diabetic nephropathy
it becomes thicker due to an increase in glomerular pressure
27
what happens to the podocytes in diabetic nephropathy
they become injured
28
what happens to the afferent and efferent arterioles in the later stages of diabetic nephropathy
they both undergo fibrosis, making the lumen smaller - this decreases the GFR
29
what are kimmelstiel-wilson nodules
fibrotic nodules that appear in the glomerulus due to too much glucose
30
what is the microalbuminuria stage of diabetic nephropathy
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
what is overt proteinuria
where the GFR falls rapidly giving systemic hypertension (due to less salt delivery to the macula densa)
32
what is given to manage diabetic nephropathy
ACE inhibitors statins change in diet and exercise
33
how do ACE inhibitors help in diabetic nephropathy
they prevent the actions of angiotensin 2 which causes an increase in permeability to proteins, mesangia expansion and construction of the efferent arteriole
34
what is hypertensive nephrosclerosis
where high blood pressure causes chronic kidney disease
35
what other signs will a patient with hypertensive nephrosclerosis have
LV hypertrophy, hypertensive eye disease
36
true or false: hypertensive nephrosclerosis develops rapidly
false - it has a slow progression
37
how is renal artery stenosis different to hypertensive nephrosclerosis
renal artery stenosis causes the hypertension whereas the chronic kidney disease is caused by the already present hypertension in hypertensive nephrosclerosis
38
what happens to the GFR in renal artery sclerosis
it falls rapidly
39
how do acute falls in blood pressure damage the kidneys
damage of the endothelium causes microangiopathic haemolytic anaemia fibrosis of the efferent arteriole leads to necrosis and RAAS activation
40
which arteriole undergoes fibrosis in hypertensive nephropathy
efferent arteriole