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Block 34 metabolic -Ellen > Haematuria PT1 > Flashcards

Haematuria PT1 Flashcards

1
Q

mortality of kidney cancer

A

40%

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2
Q

most common type of renal tumour

A

renal cell carcinoma

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3
Q

renal cell carcinoma affects

A

the proximal convoluted tubule

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4
Q

second most common form of kidney cancer

A

transitional cell carcinoma

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5
Q

describe cells of renal cell carcinoma

A
  • clear cytoplasmic polygonal cells

- with carbohydrate and lipid deposits forming yellow cells

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6
Q

inherited mutation that can cause RCC

A

von-Hippel lindau gene on 3P chromosome

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7
Q

what does mutation of the von-hippel lindau gene cause

A

increases secretion of IGF-1 growth factor upregulating expression of hypoxic-inducible factors (HIF)

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8
Q

3 genes HIF promotes the transcription of

A
  • vascular endothelial growth factor
  • platelet-derived growth factor
  • epidermal growth factor receptor
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9
Q

2 ways RCC can develop

A

sporadic

inherited

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10
Q

sporadic RCC tumours more common in

A

upper poles of kidneys in older men who have smoked

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11
Q

when does inherited von-Hippel Lindau RCC disease occur

A

younger men and women

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12
Q

inheritance pattern of Hippel Lindau RCC

A

autosomal - child with 1 parent has 50% chance of inheriting disorder

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13
Q

other organs impacted by Von-Hippel Lindau disease

A
  • retinal angiomas
  • pheochromocytomas
  • pancreatic neuroendocrine tumours
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14
Q

signs and symptoms of RCC (6)

A
  • asymptomatic
  • classic triad- haematuria, flank pain and palpable abdo mass (<10%)
  • fever & weight loss
  • anaemia
  • bone pain
  • paraneoplastic syndromes
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15
Q

paraneoplastic syndrome=

A

when tumours act as ectopic endocrine organs resulting in over-secretion of hormones

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16
Q

paraneoplastic syndromes of RCC (3)

A
  • EPO secretion
  • renin release
  • PTH-RP
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17
Q

excess PTH-RP leads to

A

hypercalcaemia

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18
Q

excess EPO leads to

A

polycytheamia

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19
Q

excess renin leads to

A

hypertension

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20
Q

in a late stage RCC what can happen to the left renal vein

A

can become compressed interrupting the venous draining of the left testies -left scrotal varicocele

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21
Q

in late stage RCC what can the tumour invade

A

IVC resulting in lower limb oedema

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22
Q

risk factors of RCC (9)

A
  • smoking
  • obesity
  • hypertension
  • age
  • male
  • PKD
  • dialysis
  • testicular/ gynaecological radiotherapy
  • family history
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23
Q

treatment of early stage RCC

A
  • partial or total local resection nephroctomy
  • radiotherapy
  • cryotherapy
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24
Q

treatment of stage 3 RCC

A
  • radical nephrectomy

- adjuvant therapy with targeted molecular therapy - Sunitinib first line

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25
Q

sunitinib=

A

tyrosine kinase inhibitor

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26
Q

adjuvant therapy of RCC stage 3 (4)

A
  • IFN-alpha monoclonal antibody
  • sunitinib
  • Bevacizumab
  • Temsirolimus
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27
Q

Treatment of RCC stage 4 (5)

A
  • targeted molecular -therapy
  • surgery
  • clinical trials
  • chemotherapy
  • palliative care
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28
Q

most common cause of malignant renal carcinomas in children under 15 =

A

Wilms disease

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29
Q

what is Wilms disease

A

a triphasic nephroblastoma

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30
Q

what does a triphasic nephroblastoma consist of (3)

A
  • metanphric blastemal cells
  • mesenchymal stromal cells
  • Epithelial cells
31
Q

a blastema=

A
  • a mass of cells capable of growth and regeneration into organs or body parts
  • undifferentiated pluripotent cells
32
Q

how does a nephroblastoma in Wilms disease occur

A

unregulated proliferation of metanephric blastemal cells

33
Q

where is a blastema seen in development

A

early stages of genitourinary developement

34
Q

mutation in Wilms disease

A

11p14 locus and WT1 tumour suppressor genen

35
Q

when does the DNA mutation happen in Wilms disease

A

pre-zygotic DNA

36
Q

pattern of the tumours in Wilms disease (4)

A
  • unilateral
  • capsulated
  • vascularised
  • do not cross midline
37
Q

precursor lesions in Wilms disease

A

nephrogenic rests (microscopic foci of primitive blastemal)

38
Q

a kidney affected by Wilm’s tumour will histologically show

A

abortive/ partly developed glomerular and tubular structures

39
Q

associations with Wilms disease

A
  • WAGR syndrome

- Beckwith-wiedemann syndrome

40
Q

signs of symptoms of Wilms disease (5)

A
  • palpable flank mass
  • abdominal distension
  • pallor (anaemia)
  • haematuria
  • hypertension
41
Q

what defines the level of the tumour in the TNM staging of renal cancer

A

gerota’s fascia (connective tissue encapsulating the kidney and adrenal gland)

42
Q

which stage does the tumour invade the renal fascia

A

T4

43
Q

5 sub-groups of RCC

A
  • clear cell
  • papillary
  • chromophobic
  • collecting duct
  • unclassified
44
Q

percentage of renal tumours that are RCC

A

80%

45
Q

4th commonest cancer in men=

A

bladder cancer

46
Q

overal mortality of bladder cancer

A

50%

47
Q

signs and symptoms of bladder cancer (5)

A
  • painless gross haematuria
  • irritative bladder symptoms
  • recurrent UTIs
  • pelvic or bone pain
  • palpable mass
48
Q

haematuria present at start of the urinary stream indicates

A

urethral damage

49
Q

risk factors for bladder cancer

A

-smoking
-occupation- aromatic dyes
-age >55 years
-pelvic radiation
-male
family history
-chronic UTIs
-schistomiasis

50
Q

chronic UTIs can lead to which type of bladder cancer

A

squamous cell carcinoma

51
Q

bladder cancers as a consequence of schistomiasis

A

simple squamous carcinoma

52
Q

spread of schistomiasis

A

contaminated water with parasites in freshwater snails

53
Q

95% of bladder cancers are

A

transitional cell carcinomas

54
Q

3 types of bladder cancer (most-least common)

A
  • transitional cell
  • squamous
  • adenocarcinomas
55
Q

why is bladder cancer more common than ureter and urethra

A

bladder is exposed to carcinogens longer with constant changing shape of transitional cells during urinary retention and micturition

56
Q

at presentation what are most TCC in the bladder

A

multifocal (more than 1)

57
Q

possible pattern of growth of TCC

A

papillary
sessile
carcinoma in situ

58
Q

TCC p53 dependant - sessile and nodular carcinomas are (4)

A
  • typically flat
  • rapidly proliferative
  • high grade
  • highly muscle invasive
59
Q

p53 independent TCC tend to be

A

non-invasive bladder cancers -papillary tumours

60
Q

squamous cell carcinoma of the bladder related to

A

schistosoma parasitic flatworm

61
Q

2 features of squamous cell carcinoma of the bladder

A
  • more invasive

- less metastatic than TCC

62
Q

where does adenocarcinoma develop in the bladder

A

glandular tissue

63
Q

cancer of the bladder muscle=

A

sarcomas

64
Q

typically metastatic spread of bladder cancer is where

A

local

65
Q

important investigations for bladder cancer

A

cystoscopy

66
Q

treatment of non-muscle invasive bladder cancer

A

TURBT- transurethral resection of bladder tumour

67
Q

how often do low grade bladder tumours undergo cystoscopic surveillance

A

5-10 years

68
Q

moderately high grade non-muscle invasive bladder tumour treatment (3)

A
  • intravesical chemo- mitomycin C cisplatin based
  • BCG immunotherapy
  • cystoscopic surveillance
69
Q

locally invasive bladder tumour treatment

A
  • radical or partical cystectomy with regional lymph node dissection
  • neoadjuvant cisplatin chemo
70
Q

metastatic disease of bladder tumour treatment

A

palliative chemo

palliative radiotherapy for local symptoms

71
Q

7 stages of bladder cancer (best to worse)

A 
Tis 
Ta 
T1
T2
T3a 
T3b
T4
72
Q

grade 1 bladder tumours =

A

well differentiated low grade

73
Q

grade 3 bladder tumours=

A

poorly differentiated with loss of original cytological appearance and high grade growth

Block 34 metabolic -Ellen (8 decks)

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