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Leila's Yr 5 Pathology (COPY) > Histopathology 3 - renal disease > Flashcards

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
Q

• Linear deposition of IgG demonstrable on glomerular basement membrane

A

Goodpasture’s syndrome

26
Q

2 examples of pauci-immune conditions

A

GPA and eGPA

27
Q

Fluorescence microscopy findings in pauci immune disease

A

Lack of/ scanty immune complex deposition

28
Q

Clinical features of pauci immune diseases

A

vasculitis everywhere

29
Q

Fluorescence microscopy findings in immune complex mediated glomerulonephritis

A

Granular/lumpy bumpY IgG immune complex deposition on GBM/mesangium

30
Q

2 main conditions which come under thrombotic microangiopathy

A

HUS and TTP

31
Q

Difference in distribution in TTP and HUS

A

HUS thrombi localised to kidneys

TTP the thrombi occur throughout circulation (esp. in CNS)

32
Q

Coombes test positive or negative in HUS/TTP

A

Negative as not AIHA

33
Q

Nephrotic syndrome triad

A

Proteinuria (>3.5g/24h), hypoalbuminaemia (<25g/L), oedema (+hyperlipidaemia)

34
Q

2 main secondary causes of nephrotic syndrome

A

Amyloidosis, diabetes

35
Q

3 main primary causes of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerular disease

36
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease

37
Q

common primary causes of nephrotic syndrome in adults

A

FSGS + membranous glomerular disease

38
Q

Minimal change disease under light microscopy

A

Glomeruli look NORMAL

39
Q

Effacement of foot processes on electron microscopy

A

Minimal change disease

40
Q

Investigation of choice for minimal change disease

A

Electron microscopy

41
Q

Management of minimal change disease

A

Generally respond to immunosuppression with steroids

42
Q

Response to steroids in FSGS

A

pOOR, ~50% RESPOND

43
Q

Minimal change disease findings on immunofluorescence

A

No immune deposits

44
Q

Membranous glomerular disease findings on immunofluorescence

A

IgG and complement in granular deposits along entire GBM

45
Q

Which ethnicity most prone to FSGS

A

Afrocarribbean

46
Q

FSGS on light microscopy

A

some glomeruli partially scarred and thickened GBM

47
Q

antibody against phospholipase A2 type M receptor (anti-PLA2R)

A

membranous glomerular disease

48
Q

Kimmelstiel-Wilson nodules

A

DIABETIC NEPHROTIC SYNDROME

49
Q

whAT IS AA amyloid derived from?

A

serum amyloid associated protein (an APP)

50
Q

What is AL amyloid derived from?

A

immunoglobulin light chains e.g. multiple myeloma

51
Q

What are the 3 possible differentials for asymptomatic haematuria?

A

Thin basement membrane disease (benign familial haematuria)
IgA nephropathy (Berger disease)
Alport syndrome

52
Q

Alpert’s syndrome symptomatic triad

A

Nephritic syndrome + sensorineural deafness + eye disorders e.g. lens dislocation/cataracts

53
Q

Inheritance of Alport’s

A

X linked

54
Q

Genetic mutation in Alport’s

A

Type IV collagen alpha-5 subunit

55
Q

Inheritance pattern of thin basement membrane disease

A

AD

56
Q

2 Most common causes of CKD

A

Diabetes, glomerulonephritis

57
Q

Lupus nephritis class II pattern of injury?

A

mesangial pattern of injury

58
Q

Lupus nephritis class III,IV,V pattern of injury?

A

Endothelial pattern of injury

59
Q

What is the commonest glomerulonephritis worldwide?

A

IgA nephropathy

Leila's Yr 5 Pathology (COPY) (100 decks)

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