Histopathology 3 - renal disease Flashcards

1
Q

what % of cardiac output do kidneys receive?

A

20%

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2
Q

Where is the blood which enters the kidney filtered?

A

the glomerulus

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3
Q

Which ion does the PCT actively reabsorb?

A

Sodium

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4
Q

What are the descending and thin ascending limb permeable and impermeable to?

A

Permeably to h2O

Impermeable to ions and urea

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5
Q

What does the ascending limb of LOH actively reabsorb?

A

Sodium and chloride

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6
Q

Which part of the kidney does aldosterone exert its affects?

A

DCT (ROMK)

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7
Q

PCKD presentation

A

haematuria, hypertension + flank pain

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8
Q

Genes involved in PCKD

A

PKD1 and PKD2

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9
Q

PCKD associated with …?

A

berry aneurysms –> SAH if ruptures

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10
Q

Patients on long term dialysis can develop…?

A

Renal cysts

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11
Q

In patients with cystic kidney disease, they are at increased risk of what cancer?

A

Papillary renal cell carcinoma

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12
Q

Most common cause of acute renal failure?

A

pre-renal

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13
Q

Renal causes of acute renal faliure

A

ATN/acute tubular injury (most common renal cause of ARF)
Acute glomerulonephritis
Thrombotic microangiopathy

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14
Q

In ATN, what are the tubular epithelial cells damaged by?

A

Toxins (contrast, Hb, myoglobin, ethylene glycol)
Ischaemia
Drugs: NSAIDs

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15
Q

Immune injury to tubules and interstitial = ?

A

Acute tubule-interstitial nephritis

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16
Q

What can cause acute tubulo-interstitial nephritis?

A

Infection + drugs e.g. NSAIDs, diuretics, PPIs, allopurinol

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17
Q

Histological features in acute tubule-interstitial nephritis

A

Interstitial inflammatory infiltrate with tubular injury, can see eosinophils and granulomas

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18
Q

Oliguria + urine casts containing erythrocytes and leucocytes

A

Acute glomerulonephritis

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19
Q

Most glomeruli on biopsy are showing a picture of crescents = ?

A

Acute crescentic glomerulonephritis

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20
Q

3 main types of acute crescentic glomuerlonephritis

A

Immune complex mediated, anti-GBM disease, pauci-immune (ANCA associated)

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21
Q

Immune complex mediated causes of acute crescentic glomerulonephritis

A

SLE, IgA nephropathy, post infectious glomerulonephritis

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22
Q

anti-GBM disease also known as

A

Goodpasture’s

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23
Q

Antibodies against what in good pasture’s?

A

type IV collagen in GBM

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24
Q

Two main organs affected in good pasture’s?

A

Lungs + kidneys

25
• Linear deposition of IgG demonstrable on glomerular basement membrane
Goodpasture's syndrome
26
2 examples of pauci-immune conditions
GPA and eGPA
27
Fluorescence microscopy findings in pauci immune disease
Lack of/ scanty immune complex deposition
28
Clinical features of pauci immune diseases
vasculitis everywhere
29
Fluorescence microscopy findings in immune complex mediated glomerulonephritis
Granular/lumpy bumpY IgG immune complex deposition on GBM/mesangium
30
2 main conditions which come under thrombotic microangiopathy
HUS and TTP
31
Difference in distribution in TTP and HUS
HUS thrombi localised to kidneys | TTP the thrombi occur throughout circulation (esp. in CNS)
32
Coombes test positive or negative in HUS/TTP
Negative as not AIHA
33
Nephrotic syndrome triad
Proteinuria (>3.5g/24h), hypoalbuminaemia (<25g/L), oedema (+hyperlipidaemia)
34
2 main secondary causes of nephrotic syndrome
Amyloidosis, diabetes
35
3 main primary causes of nephrotic syndrome
Minimal change disease Focal segmental glomerulosclerosis Membranous glomerular disease
36
Most common cause of nephrotic syndrome in children
Minimal change disease
37
common primary causes of nephrotic syndrome in adults
FSGS + membranous glomerular disease
38
Minimal change disease under light microscopy
Glomeruli look NORMAL
39
Effacement of foot processes on electron microscopy
Minimal change disease
40
Investigation of choice for minimal change disease
Electron microscopy
41
Management of minimal change disease
Generally respond to immunosuppression with steroids
42
Response to steroids in FSGS
pOOR, ~50% RESPOND
43
Minimal change disease findings on immunofluorescence
No immune deposits
44
Membranous glomerular disease findings on immunofluorescence
IgG and complement in granular deposits along entire GBM
45
Which ethnicity most prone to FSGS
Afrocarribbean
46
FSGS on light microscopy
some glomeruli partially scarred and thickened GBM
47
antibody against phospholipase A2 type M receptor (anti-PLA2R)
membranous glomerular disease
48
Kimmelstiel-Wilson nodules
DIABETIC NEPHROTIC SYNDROME
49
whAT IS AA amyloid derived from?
serum amyloid associated protein (an APP)
50
What is AL amyloid derived from?
immunoglobulin light chains e.g. multiple myeloma
51
What are the 3 possible differentials for asymptomatic haematuria?
Thin basement membrane disease (benign familial haematuria) IgA nephropathy (Berger disease) Alport syndrome
52
Alpert's syndrome symptomatic triad
Nephritic syndrome + sensorineural deafness + eye disorders e.g. lens dislocation/cataracts
53
Inheritance of Alport's
X linked
54
Genetic mutation in Alport's
Type IV collagen alpha-5 subunit
55
Inheritance pattern of thin basement membrane disease
AD
56
2 Most common causes of CKD
Diabetes, glomerulonephritis
57
Lupus nephritis class II pattern of injury?
mesangial pattern of injury
58
Lupus nephritis class III,IV,V pattern of injury?
Endothelial pattern of injury
59
What is the commonest glomerulonephritis worldwide?
IgA nephropathy