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Renal > Renal and Urological Pathology > Flashcards

Renal and Urological Pathology Flashcards

1
Q

what is nephritis and what are the 2 types?

A

inflammation of the kidney
infective (e.g pyelonephritis)
non-infective (glomerulonephritis)

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2
Q

what holds the glomerulus together?

A

mesangial cells between capillaries

visceral and parietal epithelium

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3
Q

what is glomerulonephritis and what are the main groups?

A

inflammation in the glomerulus

  • immune mediated (immune complexes in the glomerulus either due to immune complexes being directed at glomerulus or caused by circulating complexes getting stuck in the sieve of the glomerulus)
  • related to vasculitis
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4
Q

features of glomerulonephritis due to direct attack on glomerulus?

A

IgG antibodies against subunit of collagen

- good pastures syndrome

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5
Q

causes of circulating immune complexes?

A

infection (hepatitis, HIV, strep)
drugs (gold, penicillamine)
cancer (any but most often lymphomas)

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6
Q

what vasculitis can cause glomerulonephritis and what are the antibody markers?

A 
GPA = cANCA
MPA = pANCA
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7
Q

how do immune complexes cause issues?

A

they get stuck in the glomerulus sieve and clog it up, stopping it from working
disrupt the membrane charge and block membranes etc

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8
Q

what are nephrotic and nephritic syndrome?

A

clinical description of symptoms

no information about underlying cause

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9
Q

features of nephritis syndrome?

A

hypertension

haematuria

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10
Q

features of nephrotic syndrome?

A

heavy proteinuria
non-dependant oedema
hyperlipidaemia

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11
Q

protein loss includes loss of what?

A

antibodies
complement
proteins in clotting cascade

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12
Q

how is cause of glomerulonephritis diagnosed?

A

light microscopy
electron microscopy
immunoflouresence

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13
Q

what histological features can indicate rapidly progressive glomerulonephritis?

A

crescents

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14
Q

3 examples of granuloma causing disease in the kidney?

A

GPA

sarcoidosis

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15
Q

what might be seen on light microscopy in GMN?

A

hypercellularity (inflammatory cells, reactive proliferants)
sclerosis
crescents (if bad)
may see sarcoid etc if systemic disease

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16
Q

hat might be seen on electron microscopy in GMN?

A

deposits in basement membrane

  • subepithelial
  • mesangial
  • subendothelial
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17
Q

what can immunofluorescence show?

A

what kind of antibody

e.g - linear IgG at basement membrane in good pastures disease

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18
Q

what is minimal change disease?

A

type of glomerulonephritis with no known cause

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19
Q

how does minimal change present?

A

puffy face in children(nephrotic)
barely any changes on investigation
usually resolves with steroids

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20
Q

hat is FSGS?

A

type of GMN which can result from obesity, HIV, sickle cell, IV drug use

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21
Q

how does FSGS present?

A

nephritic adults

only a small area of sclerosis in some glomeruli (not all)

22
Q

what is membranous?

A

type of GMN which causes thickened basement membrane

23
Q

what causes membranous?

A 
infection (hepatitis, malaria, syphilis)
drugs (penicillamine, NSAIDs, captopril, gold)
malignancy
lupus
autoimmune disease
24
Q

presentation of membranous?

A

nephrotic syndrome
thick membranes
sub-epithelial immune deposits
variable prognosis

25
Q

what causes IgA GMN?

A

genetic
acquired defect - coeliac (as already have circulating IgA)
usually occurs post infection (strep)

26
Q

how does IgA GMN present?

A

nephritic
“smokey urine after strep infection”
IgA deposition in mesangium

27
Q

what causes membranoproliferative GMN?

A

idiopathic

type 2 = infection, lupus, malignancy (lymphoma)

28
Q

how does membranoproliferative present?

A

tram tracks - big lobulated hypercellular glomeruli with thick memrbanes (duplicated membranes)
can be nephritic or nephrotic

29
Q

ow does diabetes affect the kidney?

A

diffuse and nodular glomerulosclerosis
kimmel steil Wilson lesion (nodules)
microvascular disease (arterial sclerosis)
infection (pyelonephritis, papillary necrosis)

30
Q

what is cystic disease?

A

variety of congenital, inherited and acquired cysts

can predispose to development of cancers

31
Q

how can cancer risk of a lesion be predicted?

A

bosniak score

32
Q

what are acquired cysts>

A

benign, degenerative change in kidneys
very common
often associated with long term dialysis
simple cysts

33
Q

what are the types of polycystic kidneys?

A

AD

AR

34
Q

what is ADPCKD?

A

autosomal dominant polycystic kidney disease
due to mutation in nephrin gene (Chromosome 16 or 4)
causes lots and lots of simple thin walled cysts to develop in kidneys over time causing kidney to become huge

35
Q

secondary changes in ADPCKD?

A

haemorrhage
infection
rupture

36
Q

how can ADPCKD present?

A

large kidney - presents with mass like lesion
pain, haematuria due to rupture, infarction etc
systemic disease (liver cysts and cerebral aneurysms)

37
Q

escribe kidneys in ARPCKD?

A

kidney is normal size and has smooth surface (would hardly know there were cysts)

38
Q

how does ARPCKD present?

A 
usually in childhood (more dangerous the younger age at presentation)
systemic issues (liver cysts)
39
Q

what infection can commonly be mistaken for a malignancy in the kidney?

A

xanthogranulomatous pyelonephritis

40
Q

main benign renal tumour?

A

oncocytoma

41
Q

main malignant renal tumours?

A

chromophobe
clear cell
papillary
collecting duct

42
Q

describe features of oncocytoma?

A

small, oval and well circumscribed
mahogany brown with central stellate star
cytoplasm is very pink and granular cytoplasm

43
Q

what is a chromophobe carcinoma?

A

uncommon malignancy in the kidney

look very similar to oncocytoma but have raisonoid nuclei and perinuclear haloes

44
Q

2nd most common renal cancer?

A

papillary

generally low grade and fairly easy to remove

45
Q

what do papillary carcinomas look like?

A

finger like projections

46
Q

what is the least common renal tumour and describe prognosis

A

collecting duct carcinoma

high grade with poor prognosis

47
Q

what is the most common renal cancer and how does it present?

A

clear cell carcinoma
haematuria
mass
hypertension sometimes

48
Q

risk factors for clear cell carcinoma?

A

obesity

genetic influence

49
Q

what does clear cell carcinoma look like?

A

very yellow surface
partly cystic and very heterogenous surface
presence of clear cells

50
Q

how is clear cell carcinoma staged?

A

size then invasion of other structures (usually renal vein)

51
Q

where can cell carcinomas often invade?

A

grow into renal vein, up into IVC and grow up towards the heart

52
Q

what genotype is associated with renal cancers and why?

A

VHL
VHL codes for HIF (hypoxia inducible factor)
normally VHL ubiquitinates HIF (inactivates it by adding ubiquinate)
in low O2 they dissociate and HIF acts as a transcription factor for VEGF, PDGFRB and EPO

Renal (34 decks)

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