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CP reviewer 1 > Urological Pathology > Flashcards

Urological Pathology Flashcards

1
Q

What are the 2 major types of renal cancers?

A
  1. Renal Cell Carcinoma (RCC)

2. Wilms’ Tumour

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2
Q

What is a renal cell carcinoma? Where does it arise from?

A

Cancer of the kidney that arises from the renal tubular epithelium

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3
Q

What are the 2 most common types of RCC?

A
  1. Clear cell (75%)

2. Papillary (10%)

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4
Q

Which aspect of family history can predispose people to RCC?

A

VHL gene:

Von Hippel-Lindau syndrome - a hereditary condition associated with tumours arising in multiple organs.

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5
Q

Aetiology and pathogenesis for RCC?

A
  • Environmental factors causing genetic mutations e.g. smoking
  • Inherited genetic mutations e.g. VHL gene

These mutations accumulate –> ‘hallmarks of cancer’ accumulate –> malignant cell

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6
Q

The effects of cancers can be:

1) Local primary effects of tumour
2) Effects of distant metastases
3) Paraneoplastic syndromes: signs and symptoms that are NOT related to local effects of the primary of metastatic tumours.

How can paraneoplastic syndromes develop?

A

These develop as a result of either:

a. Proteins/hormones secreted by the tumour cells
b. Immune cross reactivity between tumour cells and normal tissues

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7
Q

What are the primary effects of RCCs?

A

 Haematuria

 Abdominal pain

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8
Q

What are the 2 most common locations of distant metastases in RCCs? What are their effects here?

A

 Lung mets (‘cannonball metastases) –> SOB etc

 Bone mets –> Bone pain etc

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9
Q

What paraneoplastic syndromes can RCCs lead to?

A
  • Weight loss (‘cancer cachexia)
  • Hypertension
  • Polycythaemia
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10
Q

How can RCCs cause hypertension?

A

o Kidneys produce renin which regulates blood pressure

o Increased renin production from tumour causes hypertension

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11
Q

How can RCCs lead to polycythaemia?

A

Tumour produces erythropoietin (stimulates production of RBCs)

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12
Q

Define polycythaemia?

A

a high concentration of RBCs in your blood

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13
Q

What is a Wilms’ tumour? What is it also known as?

A

Nephroblastoma

Cancer of the kidney that arises from nephroblasts (cells that develop into the kidney in embryological development)

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14
Q

Epidemiology of Wilm’s tumour?

A 
• Children under 5 
• 5-10% associated with genetic syndromes:
o	Beckwith-Weidemann Syndrome 
o	WAGR Syndrome
o	Denys-Drash Syndrome
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15
Q

What are common features of Beckwith-Weidemann Syndrome?

A

The most common features include macrosomia (large body size) and macroglossia (large tongue)

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16
Q

Mutations in which gene can lead to Wilm’s tumour and Denys-Drash Syndrome etc?

A

WT1

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17
Q

For Wilms’ tumours, what are the:

1) Local primary tumour effects
2) Effects of distant metastases
3) Paraneoplastic syndromes?

A

1) a. Abdominal distention (especially if bilateral – 10% of Wilms’ Tumours are bilateral)
b. Haematuria

2) Mets are rare
3) PNS are rare

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18
Q

What is urolithiasis?

A

Stones forming in the lumen of the urinary tract, anywhere from renal calyx to the bladder.

Aka urinary tract calculi/stones.

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19
Q

What are the different types of urinary stones?

A
  • Calcium stones (70%)
  • Urate stones (5%)
  • Cystine stones (1%)
  • Struvite stones (15%) (magnesium ammonium phosphate)
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20
Q

What is the aetiology of:

1) calcium stones
2) urate stones
3) cystine stones
4) struvite stones

A

1) hypercalcaemia
2) gout, malignancy (high cell turnover)
3) congenital cystinuria (kidneys unable to reabsorb amino acids)
4) UTI with a bacteria that can produce urease e.g. proteus

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21
Q

What is congenital cystinuria ? What types of urinary stones can it lead to?

A

Cystinuria is a rare hereditary kidney disorder that results in excretion of the amino acid cystine into the urine due to kidneys being unable to reabsorb them, often causing cystine stones to form in the urinary tract.

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22
Q

For a UTI to cause struvite stones, what bacteria must it be?

A

a bacteria that can produce urease e.g. proteus

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23
Q

Pathogenesis of calcium, urate and cystine stones:

A
  1. Too high a concentration of soluble material
  2. Urine becomes saturated
  3. Soluble material precipitates out
  4. Stones form
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24
Q

Pathogeneis of struvite stones:

A
  1. UTI with urease producing bacteria e.g. proteus
  2. Urease converts urea to ammonia
  3. Ammonia causes pH to rise
  4. Precipitation of magnesium ammonium phosphate salts
  5. Stones form
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25
Q

How does a bacteria that can produce urease lead to struvite stones?

A

Urease converts urea to ammonia

Ammonia causes pH to rise

Precipitation of magnesium ammonium phosphate salts

Stones form

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26
Q

The pain from urolithiasis depends on the location of the stone. Where does the pain present with:

1) Ureter stones
2) Bladder stones
3) Urethra stones

A

o Ureter: ‘loin to groin’ pain (aka renal colic)
o Bladder: lower abdominal pain
o Urethra: dysuria

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27
Q

Why does urolithiasis present with haematuria?

A

Due to stone scratching off epithelium

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28
Q

How do calcium urinary stones appear on xrays?

A

radio opaque therefore can see on x-ray and shows up as white dense area.

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29
Q

How do cystine and urate stones appear on xrays?

A

Tend not to be visible

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30
Q

How can urolithiasis lead to hydronephrosis and hydroureter?

What is the end result of this?

A

Stone can get stuck in urinary tract and cause obstruction:

  • Ureter gets more distended and so does kidney due to blockage
  • Leads to hydronephrosis (swelling of kidney(s) due to build-up of urine) +/- hydroureter (dilation of ureter(s) due to obstruction of urine outflow)

Eventually leads to renal impairment due to pressure on kidney

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31
Q

How can urolithiasis lead to infection?

A

Due to urinary stasis if there is a blockage

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32
Q

How can urolithiasis lead to SCC risk?

A

Local trauma caused by stone causes squamous metaplasia (transitional turns into squamous epithelium in order to deal with trauma) –> SCC risk

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33
Q

What is Vesicoureteral Reflux (VUR)?

A

When the bladder contracts, the urine flows backwards from the bladder to the ureter rather than from the bladder to the urethra.

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34
Q

Who does Vesicoureteral Reflux (VUR) tend to affect??

A

Young people, especially those under 2

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35
Q

Aetiology of Vesicoureteral Reflux (VUR)?

A

Congenital abnormality of vesicoureteric junction

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36
Q

What is the vesicoureteric junction?

A

the most distal portion of the ureter where it connects to the bladder

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37
Q

How does an abnormality of vesicoureteric junction lead to Vesicoureteral Reflux (VUR)?

A
  • Ureter enters bladder at an abnormal angle –> shorter intramural ureter
  • When draining, muscle in bladder wall contracts but there is not enough muscle in contact with ureter to compress it –> ureter remains patent –> urine flows the wrong way
38
Q

Clinical features of Vesicoureteral Reflux (VUR)?

A 
• Usually asymptomatic 
• Most children ‘grow out of it’
• Only symptoms of complications:
- Urinary stasis --> UTI
- Back pressure building up in kidney and ascending infection can lead to renal damage: Hydronephrosis and hydroureter
39
Q

What is urothelial carcinoma?

A

Cancer of urothelial epithelium aka transitional cell carcinoma

40
Q

Who is urothelial carcinoma most common in?

A

Older men

41
Q

Common symptom of urothelial carcinoma?

A

Haematuria

42
Q

Causes of urothelial carcinoma?

A

Environmental causes tend to play a larger role than inherited mutations:

  • Smoking
  • Exposure to certain chemicals e.g. arylamines
43
Q

Clinical features of urothelial carcinoma can be:

1) Local primary tumour effects
2) Effects of distant metastases
3) Paraneoplastic syndromes: PNS

Describe each of these for urothelial carcinoma

A

1) a. Haematuria
b. Frequency, urgency, dysuria
c. Urinary obstruction

2) a. lung mets –> SOB etc
b. Bone mets –> Bone pain etc
c. Liver mets –> jaundice etc

c) PNS are rare

44
Q

What is neurogenic bladder?

A

Inability to properly empty the bladder due to neurological damage.

Damage to any points in neuron pathway can lead to cause inability to empty bladder properly.

45
Q

What are the 2 types of neurogenic bladder?

A
  1. Spastic

2. Flaccid

46
Q

What is the cause of ‘spastic’ neurogenic bladder?

A

if damage to brain or spinal cord (upper motor neuron)

47
Q

What is the cause of ‘flaccid’ neurogenic bladder?

A

if damage to peripheral nerves (lower motor neuron)

48
Q

What can cause UMN damage that can lead to neurogenic bladder?

A

Stroke, MS, spinal injury

49
Q

What is MS?

A

An autoimmune demyelinating disorder –> immune system attacks the insulating fat in the brain and causes plaques

Transmission of impulses is poor

50
Q

What can cause LMN damage that can lead to neurogenic bladder?

A

Pregnancy, diabetes, alcohol abuse

51
Q

How can alcohol abuse lead to LMN damage?

A

B12 deficiency - B12 needed for good nerve health

52
Q

How can pregnancy lead to LMN damage?

A

Big uterus presses on nerves in pelvis

53
Q

How can diabetes lead to LMN damage?

A

Affects peripheral nerves (including those controlling continence)

54
Q

What is the bladder stretch reflex?

A

The bladder stretch reflex is a primitive spinal reflex, in which micturition is stimulated in response to stretch of the bladder wall.

During toilet training in infants, this spinal reflex is overridden by the higher centres of the brain, to give voluntary control over micturition.

55
Q

Describe the reflex arc in the bladder stretch reflex

A
  1. Bladder fills with urine, and the bladder walls stretch. Sensory nerves detect stretch and transmit this information to the spinal cord.
  2. Interneurons within the spinal cord relay the signal to the parasympathetic efferents (the pelvic nerve).
  3. The pelvic nerve acts to contract the detrusor muscle, and stimulate micturition.

This is non functional post childhood.

56
Q

Describe the effect on the bladder reflex in a spinal cord lesion above T12

A

In this case, the afferent signals from the bladder wall are unable to reach the brain, and the patient will have no awareness of bladder filling. There is also no descending control over the external urethral sphincter, and it is constantly relaxed.

There is a functioning spinal reflex, where the parasympathetic system initiates detrusor contraction in response to bladder wall stretch. Thus, the bladder automatically empties as it fills – known as the reflex bladder.

57
Q

Describe the effect on the bladder reflex in a spinal cord lesion below T12

A

Flaccid bladder:

A spinal cord transection at this level will have damaged the parasympathetic outflow to the bladder. The detrusor muscle will be paralysed, unable to contract. The spinal reflex does not function.

In this scenario, the bladder will fill uncontrollably, becoming abnormally distended until overflow incontinence occurs.

58
Q

What are the clinical features of neurogenic bladder?

A

• Symptoms related to lack of control of bladder emptying: Urinary retention +/- abdominal distention, incontinence, urge, frequency

• Symptoms related to complications:
o Stasis –> UTI –> dysuria etc
o Stasis –> urinary stones –> haematuria etc
o Inability to empty bladder –> bladder distention –> hydroureter –> hydronephrosis –> renal function impairment –> oedema etc

59
Q

What is Benign Prostatic Hyperplasia (BPH)?

A

Increased number of both stromal and glandular cells in the prostate. Known by patients as an ‘enlarged prostate’.

60
Q

Who is BPH most commonly seen in?

A

Old men (20% by age 40 vs 70% by age 60)

61
Q

What is the effect of BPH on the urethra? What are the knock-on effects of this?

A

Compression of urethra –> obstruction of bladder outlet

This can cause:
1) urinary stasis –> infection or stones

2) Back pressure –> renal damage
3) Acute urinary retention

62
Q

How can BPH affect detrusor muscle of bladder?

A

BPH can lead to detrusor muscle hypertrophy as bladder has to work extra hard to try and force urine through narrowed urethra (narrowed due to BPH).

63
Q

Clinical features of BPH?

A 
Lower urinary tract symptoms (LUTS):
o	Hesitancy or urgency
o	Poor/ intermittent stream
o	Straining
o	Prolonged micturition
o	Incomplete bladder emptying
o	Dribbling
o	Frequency
o	Incontinence
o	Nocturia
64
Q

What is Prostatic Adenocarcinoma?

A

Cancer of the glandular epithelium in the prostate.

65
Q

When genes are associated with prostatic adenocarcinoma?

A

BRCA 1/2

66
Q

Who is prostatic adenocarcinoma most commonly seen in?

A
  • Old men (major risk factor)
  • Black men
  • Family history (inc BRCA1/2)
  • Pesticide exposure
67
Q

Why is BPH and prostatic adenocarcinoma often seen in the same patients?

A

As the main risk factor for BPH is also age, the two are often seen in the same patients, but BPH is NOT a precursor to cancer.

68
Q

For prostatic adenocarcinoma, what are the:

1) Local primary tumour effects
2) Effects of distant metastases
3) Paraneoplastic syndromes

A

1) Lower urinary tract symptoms (LUTS) (hesitancy, dribbling etc)
2) Bone mets –> bone pain
3) PNS are rare

69
Q

What is cryptorchidism?

A

Aka undescended testis. Where the testis is NOT in the scrotum.

Types based on site of testis.

70
Q

Who is cryptorchidism most commonly seen in?

A

Premature babies (but still present in 3% of those born full term)

71
Q

Environmental and genetic causes of cryptorchidism?

A

Multifactorial - often no cause identified

Genetic:

  • FH
  • Downs Syndrome
  • Kleinfelter syndrome

Environmental:

  • Low birth weight
  • Maternal smoking
  • Maternal alcohol
  • Prematurity
72
Q

Describe normal descent of embryological testes

A

7 weeks: testes begin to form in abdomen

10-15 weeks: transabdominal descent

25-35 weeks: inguinoscrotal descent

73
Q

Clinical features of cryptorchidism?

A
  • Empty scrotum (10% bilateral)
  • May resolve spontaneously
  • May develop complications
  • Infertility
  • Hernias
  • Testicular cancer risk
  • Testicular torsion
74
Q

What is a seminoma?

A

Malignant neoplasm of the testis arising from germ cells (responsible for making sperm) in the seminiferous tubules.

75
Q

What is the most common type of testicular cancer?

A

Seminoma

76
Q

Who is seminomas most seen in?

A

• Young men (25-45 YO)
• Family history
• Cryptorchidism
–> REGARDLESS OF WHETHER IT WAS SURGICALLY CORRECTED OR ONLY AFFECTED THE OTHER TESTIS

77
Q

What gene is often implicated in seminomas?

A

KIT gene

78
Q

Local primary effects of seminomas?

A

Testicular lump, swelling, pain etc

79
Q

Effects of distant metastases of seminomas?

A

a. lung mets –> SOB etc

b. Lymph nodes mets –> back pain

80
Q

Which paraneoplastic syndrome can seminomas lead to?

A

Gynecomastia

81
Q

What is gynecomastia?

A

An enlargement or swelling of breast tissue in males. It is most commonly caused by male oestrogen levels that are too high or are out of balance with testosterone levels.

82
Q

What kidney problems can lead to obstruction of urinary tract?

A

Tumours (if large)

83
Q

What ureter problems can lead to obstruction of urinary tract?

A

MATERIAL IN LUMEN
Calculi
Clots
Sloughed papillae

WALL ABNORMALITIES
Stricture
Tumour
Congenital abnormalities

EXTERNAL COMPRESSION
Pregnancy
Cervical/ colon Ca
Retroperitoneal fibrosis
AAA

FUNCTIONAL
VUJ reflux*

84
Q

What penis problems can lead to obstruction of urinary tract?

A
  • Tumour

- Phimosis

85
Q

What urethra problems can lead to obstruction of urinary tract?

A

Stricture
Foreign body
Posterior urethral valves
Blocked catheter

86
Q

What prostate problems can lead to obstruction of urinary tract?

A

BPH
Tumours
Prostatitis

87
Q

What bladder problems can lead to obstruction of urinary tract?

A 
Calculi
Tumours
Neurogenic bladder*
Anticholinergic drugs*
Constipation
88
Q

What renal pelvis problems can lead to obstruction of urinary tract?

A

Staghorn calculi

Tumours

89
Q

How can complete urinary tract obstructions present?

A

Anuria

Pain

90
Q

How can partial urinary tract obstructions present?

A

Often asymptomatic

91
Q

What complications can urinary tract obstructions lead to?

A

Back pressure:
o Irreversible renal impairment
o Secondary VUR

Urinary stasis:
o Infection
o Calculi formation

CP reviewer 1 (59 decks)

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