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MED4 ACP > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

Compare 2 patterns of pathogenesis of glomerular injuries (HSR type, Model, IF pathology, examples)

A

Pathogenesis: type III; type II
Reflect by: Heymann model; Masugi model
IF: granular; linear
Diseases: most GN; Goodpasture syndrome

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2
Q

Aetiology of glomerulonephritis (2+3+3+1)

A

Primary:
- nephrotic: minimal change disease, membranous nephropathy
- nephritic: IgA nephropathy, post-Streptococcal GN, Rapidly progressive / Crescentic GN
Secondary:
- Diabetic nephropathy, Lupus nephritis, Amyloidosis
Hereditary: Alport syndrome

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3
Q

MC nephrotic syndrome in children

A

Minimal change disease

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4
Q

Which GN presents with selective proteinuria?

A

Minimal change disease

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5
Q

GN pathology: diffuse effacement of podocyte foot processes

A

Minimal change disease

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6
Q

Treatment for minimal change disease

A

Steroid

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7
Q

MC nephrotic syndrome in adults

A

Membranous nephropathy

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8
Q

Which autoAbs (2) are associated with membranous nephropathy?

A

autoAb against PLA2R, THSD7A

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9
Q

Secondary causes for membranous nephropathy (5)

A

Infection (e.g. HBV, HCV, syphilis, malaria)
Malignancy
Autoimmune
Drugs (e.g. ACEI, penicillamine)
Heavy metals

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10
Q

Pathology of membranous nephropathy (4)

A

LM: diffuse GBM thickening
IF: granular pattern
EM: subepithelial deposits, spike and dome pattern

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11
Q

MC detected immunoglobulin and complement in IF for GN

A

IgG, C3

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12
Q

Compare nephrotic and nephritic syndrome (pathogenesis, presentations (6 vs 5))

A

Pathogenesis: ↑ permeability to glomeruli to plasma protein v.s. inflammation of glomeruli –> capillary wall injury –> decrease GFR
Presentations
- Nephrotic: proteinuria (>3.5g/day), hypoalbuminaemia, generalised oedema, hyperlipidaemia, hypercaogulability, hypertension
- Nephritic: proteinuria (0.15~3.5g/day), haematuria, oliuria / azotaemia, hypertenion, oedma

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13
Q

Prognosis of membranous nephropathy

A

1/3 resolve, 1/3 persist, 1/3 progress

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14
Q

Timing of GN: post-streptococcal GN vs IgA nephropathy

A

Post-streptococcal GN: 1~4 weeks
IgA nephropathy: 1~2 days

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15
Q

Pathology of post-streptococcal GN (4)

A

LM: diffuse capillary proliferation, leukocytic infiltration
IF: granular pattern
EM: subepithelial “humps”

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16
Q

Prognosis of post-streptococcal GN

A

95% spontaneous recovery

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17
Q

MC nephritic syndrome

A

IgA nephropathy

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18
Q

Pathogenesis of IgA nephropathy

A

production of mutated GD-IgA, which is not degraded, after mucosal infection –> recognised as foreign antigens & autoAb form –> IC form & deposit in mesangium

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19
Q

What is Henoch-Schonlein Purpura (HSP)?

A

systemic syndrome involving IgA nephropathy, purpuric rash…

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20
Q

Pathology of IgA nephropathy

A

mesangial deposition of IgA

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21
Q

3 types of crescentic GN

A
  1. Anti-GBM Ab-mediated
  2. IC-mediated
  3. Pauci-immune type (associated with ANCA)
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22
Q

Presentations of Goodpasture disease

A

haemoptysis, acute renal failure

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23
Q

Antibodies in Goodpasture disease

A

anti-a3(IV)NC1
(Ag found in basement membrane of alveoli & glomeruli)

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24
Q

Management of Goodpasture disease (2)

A

plasma exchange
immunosuppression

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25
Q

Vasculitis associated with crescentic GN (2)

A

microscopic polyangiitis
granulomatosis with polyangiitis

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26
Q

Pathology of crescentic GN (2)

A

crescents (extracapillary proliferation)
ruptures in GBM

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27
Q

MC glomerulonephropathy

A

diabetic nephropathy

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28
Q

Pathogenesis of diabetic nephropathy

A

hyperglycaemia –> glycation of protein at efferent arterioles (hyaline arteriosclerosis) –> ↑ pressure of glomeruli –> GBM thickening, mesangial expansion –> losing anionic charge & podocyte damage –> albuminuria

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29
Q

Pathology of diabetic nephropathy (4)

A
  • Diffuse GBM thickening
  • Diffuse mesangial expansion
  • Nodular mesangial sclerosis (Kimmelstiel-Wilson lesion)
  • mesangiolysis
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30
Q

Pathogenesis of lupus nephritis

A

cell damage –> ↑ anti-nuclear Ab –> IC formation & deposition

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31
Q

Most severe form (also MC) of lupus nephritis

A

diffuse proliferative

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32
Q

Causes of diffuse proliferative GN (2)

A

lupus nephritis, post-streptococcal GN

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33
Q

Pathology of lupus nephritis

A

“full house” IC by IF

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34
Q

MC genetic mutation for Alport syndrome (hereditary pattern)

A

COL4α5 (X-linked)

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35
Q

Presentations of Alport syndrome (4)

A
  • nephritis
  • sensorineural deafness
  • lens dislocation, cataract
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36
Q

Pathology findings in urine for nephrotic syndrome

A

fatty casts

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37
Q

GN pathology: GBM thickening (2)

A

membranous nephropathy, diabetic nephropathy

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38
Q

GN pathology: subepitheial deposits (2)

A

membranous nephropathy, post-streptococcal GN (subepithelial “humps”)

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39
Q

GN pathology: spike and dome pattern

A

membranous nephropathy

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40
Q

GN pathology: mesangial abnormalities

A
  • IgA nephropathy (mesangial deposits)
  • Diabetic nephropathy
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41
Q

GN pathology: rupture in GBM

A

crescentic GN

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42
Q

GN pathology: “basketweave”/ “bread crumb” appearance

A

Alport syndrome

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43
Q

GN pathology: splitting of lamina densa

A

Alport syndrome

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44
Q

Aetiology of tubulo-interstitial nephritis (1+2+2+3)

A
  • Acute tubular necrosis
  • Acute pyelonephritis, Kidney tuberculosis
  • Drug-induced TIN, analgesic nephropathy
  • Obstructive nephropathy, radiation nephropathy, renal transplant rejection
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45
Q

Pathology of acute tubular necrosis (1+3)

A

Gross: pale enlarged kidney
Histology:
- granular casts
- interstitial oedema
- necrosis

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46
Q

Pathology of acute pyelonephritis (2)

A
  • enlarged kiney, with yellow abscesses on kidney surface
  • neutrophil infiltrate in tubules and interstitium
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47
Q

Pathology of kidney TB (2)

A
  • multiple cavities with yellow necrotic materials
  • extensive caseous necrosis, granulomas
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48
Q

Examples of drugs inducing GN

A

penicillin, septrin, NSAIDs, thiazides, cimetidine…

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49
Q

Pathology of drug-induced GN (3)

A
  • mononuclear cell infiltrate
  • Type I HSR: eosinophils
  • Type IV HSR: non-necrotizing granuloma
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50
Q

What is analgesic nephropathy?

A

dose-depdent oxidative injury caused by combined chronic use of aspirin + paracetamol

51
Q

Pathology of analgesic nephropathy (3)

A

papillary necrosis, tubular atrophy, interstitial fibrosis

52
Q

MC adult renal cyst

A

Simple renal cyst

53
Q

MC children renal cyst

A

cystic renal dysplasia

54
Q

Pathogenesis of adult PKD

A

PKD1 mutation (AD) –> failure to produce polycystin –> ciliopathy –> aberrant signalling pathway –> abnormal cell proliferation –> multiple enlarging bilateral cysts

55
Q

Presentations (3), complications (2), and associations (3) of adult PKD

A

Presentations:
- flank pain
- heavy, dragging sensation
- haematuria
Complications: hypertension, UTI
Associations: hepatic cysts, Berry aneurysm, MVP

56
Q

Pathogenesis of juvenile PKD

A

PKHD1 gene mutation –> fail to produce fibrocystin (regular of polycystin)

57
Q

Tumour-like lesion (1) and tumours (6) found in kidneys

A
  • ## Xanthogranulomatous pyelonephritis
  • Oncocytoma
  • Papillary adenoma
  • ## Angiomyolipoma
  • RCC (MC)
  • TCC
  • Wilm’s tumour (MC in children)
58
Q

Lifetime risk of prostate cancer

59
Q

Risk factors for prostate cancer (3)

A

Ageing, smoking, hormone, genetics

60
Q

Gene mutation for CA prostate

A

TMPRSS2/ERG fusion

61
Q

Precursor lesion of CA prostate and its feature

A

prostate intraepithelial neoplasia (PIN)
(basal cells still intact)

62
Q

How much proportion of CA prostate is palpable and what is its indication on staging?

63
Q

Presentations of CA prostate (4)

A

(symptoms are often late findings)
- obstructive LUTS
- haematuria, haemospermia, early-onset erectile dysfunction

64
Q

3 common sites of metastasis from CA prostate

A

bone, liver, adrenal

65
Q

PSA normal range

66
Q

Grading score for CA prostate after biopsy. Describe in brief.

A

Gleason score, the sum of 2 most predominant histological patterns in prostate biopsy (=> Grade 1~5)

67
Q

3 criteria in determining the staging of CA prostate

A

TNM, serum PSA, Gleason score

68
Q

Management of CA prostate (3+3)

A

Local: active surveillance, radical prostatectomy, radiotherapy
Metastatic: surgical / medical castration, chemotherapy, androgen receptor targeted agents (ARTA)

69
Q

Which type of carcinoma is MC for CA prostate?

A

adenocarcinoma

70
Q

Which zone is CA prostate located at?

A

peripheral zone (so palpable in T2 but obstruct in late stage)

71
Q

MC cause of enlarged prostate >50y

72
Q

Pathogenesis of BPH

A

↑ sensitivity of prostate tissue to DHT –> stromal hyperplasia

73
Q

Which zone is BPH located at?

A

transitional zone (so obstruct quickly)

74
Q

DRE result for BPH (4)

A

smoothly enlarged, non-tender, >3 finger breath, anal tone intact

75
Q

Complications of BPH (1+3+2)

A

Prostate level: bleeding / haematuria
Region level: AROU, recurrent UTI, bladder stone
Kidney level: hydronephrosis, obstructive nephropathy
!! ⨉ CA prostate

76
Q

Imaging tools for BPH (3)

A

Plain AXR/KUB, transrectal ultrasound, cystoscopy

77
Q

Pathology of BPH (3)

A

nodular hyperplasia
glandular and fibromuscular proliferation
basal cells still intact

78
Q

Managmenet for BPH (1+2+3)

A

Conservative: lifestyle modifications
Medial:
1. alpha blocker (e.g. tamsulosin)
2. 5 α -reductase inhibitor (e.g. finasteride)
Surgical:
1. UroLift
2. Steam treatment
3. TURP (transurethral resection of prostate)

79
Q

Aetiology & Treatment of xanthogranulomatous pyelonephritis

A

Aetiology: urinary tract obstruction –> recurrent bacterial infection
Treatment: antibiotics –> nephrectomy

80
Q

Which benign renal neoplasm is difficult to differentiate from RCC? What can determine a neoplasm to be RCC?

A

Oncocytoma
non-distinguishable unless there is evidence of metastasis or infiltration into adjacent structures

81
Q

Which renal tumour gives peritoneal bleeding as a common side effect?

A

Angiomyolipoma

82
Q

Origin of angiomyolipoma

A

perivascular epithelioid cells (vessels, smooth muscles, fat)

83
Q

Genetic disorder associated with renal angiomyolipoma (2 genes related) (hereditary pattern)

A

Tuberous sclerosis (TSC1, TSC2) (AD)

84
Q

Risk factors for RCC (3+5)

A

Lifestyle: smoking, obesity, occupation (petrol)
Underlying conditions: HT, CKD, PKD, acquired cystic disease, renal transplant

85
Q

Pathogenesis for von-Hippel-Lindau disease

A

VHL mutation (AD) –> impaired degradation of HIF α (hypoxia inducible factor) –> tumorigenesis

86
Q

von-Hippel-Lindau disease presentations / tumour association

A

Haemangioblastoma, renal clear cell carcinoma, phaeochromocytoma, pancreatic neuroendocrine tumour, endolymphatic sac tumour [inner ear], liver cysts

87
Q

Hereditary syndromes associated with RCC (4)

A

**von Hippel-Lindau syndrome
Hereditary leiomyomatosis & renal cell cancer (HLRCC)
Hereditary papillary renal carcinoma (HPRC)
Brit-Hogg-Dube (BHD) syndrome

88
Q

Presentations of RCC (triads + 4 paraneoplastic)

A
  • haematuria, flank pain, palpable renal mass
  • anaemia, HHM, polycythaemia, HT
89
Q

5 types of RCC

A

Clear cell carcinoma, Papillary cell carcinoma, Chromophobes carcinoma, Collecting duct carcinoma, Xp11 translocation carcinoma

90
Q

Staging and grading (2) of RCC

A
  1. TNM staging
    (T1: <7cm within kidney, T2: >7cm within kidney, T3: extend into perinephric tissues / major veins, T4: beyond Gerota’s fascia)
  2. Fuhrman grading (nuclear size)
  3. WHO grading (nucleoli prominance)
91
Q

Treatment for RCC (1+4)

A

Local: Partial / Radical nephrectomy
Metastatic: anti-VEGF-r (sunitinib, sorafenib, pazopanib, axitinib…)

92
Q

MC primary renal tumour in children

A

Wilms tumour

93
Q

Precursor lesion of Wilms tumour

A

nephrogenic rests / cysts

94
Q

Hereditary syndromes (3) associated with Wilms tumour and their genes

A

(WT1) WAGR syndrome, Danys-Drash syndrome
(WT2) Beckwith-Wiedemann syndrome

95
Q

Prognosis of Wilms tumour

A

90% cure with treatment

96
Q

Pathology of Wilms tumour (gross and microscopic)

A

Gross: very large, pale-grey, soft tumour
Microscopic: triphasic (blastemal, stromal, epithelial)

97
Q

Urinary bladder: aetiology of squamous metaplasia vs glandular metaplasia

A

squamous: schistosomiasis, stones
glandular: chronic cystitis

98
Q

Types of bladder cancer (4)

A

Transitional cell carcinoma
Squamous cell carcinoma
Adenocarcinoma
Rhabdomyosarcoma

99
Q

MC sarcoma in children

A

Rhabdomyosarcoma

100
Q

Risk factors for bladder cancer (TCC vs SCC vs ADC vs Rhabdomycosarcoma) (4+2+1+1)

A

TCC: smoking, occupation, cyclophosphamide, genetics
SCC: schistosomiasis, bladder stone
ADC: chronic cystitis
Rhabdomyosarcoma: urachal remnants

101
Q

Genetic risk factors for transitional cell carcinoma in urinary bladder (2)

102
Q

Features of p53-dependent TCC bladder (2)

A

flat, more invasive

103
Q

Imaging for bladder cancer (2)

A

Flexible cystoscopy +/- biopsy
CT urogram

104
Q

TNM staging for TCC bladder (6)

A

Ta: non-invasive papillary carcinoma
Tis: non-invasive flat carcinoma in situ
T1: invading lamina propria
T2: invading muscularis propria
T3: invading perivesical fat
T4: invading adjacent structures

105
Q

Which is the only tumour that is considered malignant even without stromal invasion?

A

Bladder cancer

106
Q

What is field effect? What is the associated cancer?

A

Bladder cancer. Entire urothelium is affected by genetic changes that give rise to tumorigenesis –> recurrence is inevitable

107
Q

WHO/ISUP grading for bladder cancer (4)

A
  1. Papilloma
  2. Papillary urothelial neoplasm of low malignant potential
  3. Low-grade papillary urothelial carcinoma
  4. High-grade papillary urothelial carcinoma
108
Q

Management for bladder cancer (2)

A

Non-muscle invasive: TURBT (transurethral resection of bladder tumour)
Muscle invasive: radical cystectomy + urinary diversion

109
Q

TNM staging for CA prostate (4)

A

T1: clinically undetectable
T2: palpable on DRE
T3: invade beyond prostatic capsule
T4: invade adjacent structures

110
Q

Precursor lesion of germ cell tumours

A

germ cell neoplasm in situ (GCNIS)

111
Q

Seminoma vs NSGCT (presents at…, spread, RT response)

A

Presents at: early stage ; late stage
Spread: lymphatic ; hematogenous
RT: sensitive ; resistant

112
Q

4 types of NSGCT (age & origin)

A

Embryonal CA (30s), Choriocarcinoma (20s, trophoblast), Yolk sac tumour (<4, endoderm), teratoma (any, trigeminal layers)

113
Q

Seminoma: age, origin, pathology (4), markers (2)

A

Age: 40s
Origin: seminiferous tubule
Pathology:
- white-yellow “potato”
- clear cells in sheets or tubules
- lymphocytes
- granuloma
Markers:
- PLAP
- Oct-4

114
Q

Embryonal CA: pathology, markers (3)

A

Pathology: variegated tumour
Markers: PLAP, Oct-4, CD30

115
Q

Tumour markers for choriocarcinoma and yolk sac tumour respectively

116
Q

GCT vs Sex cord stromal tumours (prevalence, malignancy)

A

Prevalence: 95%; 5%
Malignancy: malignant, benign

117
Q

What are the two types of sex cord-stromal tumour?

A

Leydig cell tumour, Sertoli cell tumour

118
Q

Leydig cell tumour vs Sertoli cell tumour (colour, histology, hormonal activity)

A

Colour: tan-brown; white-yellow
Histology: eosinophils, Reinke crystals; tubular structures
Hormonal activities: yes (gynaecomastia, sexual precocity); varies

119
Q

Staging for testicular tumour

A

TNMS Staging (S stands for serum tumour marker)

120
Q

3 stages of testicular tumour

A

I: testis, spermatic cord
II: LN below diaphragm
III: LN above diaphragm
⨉ stage IV

121
Q

Investigations for prostate cancer

A

PSA
PHI
Prostate biopsy (“Fusion biopsy”, transrectal / transperineal)
Multiparametric MRI prostate

122
Q

What is Gleason score?

A

sum of 2 most predominant histological patterns in prostate biopsy

1 is most well-differentiated, 5 is most poorly differentiated

It is a key prognostic factor of CA prostate

123
Q

Which RCC is associated with MET gene?

A

Papillary RCC

MED4 ACP (13 decks)

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