urogenital Flashcards

1
Q

what is urolithiasis and its primary cause?

A

formation of a calculus or calculi (stones) within the urinary tract
- due to stasis
- supersaturation of urine with crystalline material (calcium salt)

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2
Q

secondary causes of urolithiasis?

A
  1. UTI
  2. catheter or foreign body in the bladder
  3. vit A deficiency producing squamous metaplasia of upper urinary tract mucosa
  4. low urinary PH predisposes to formation of uric acid stones
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3
Q

types of renal calculi

A
  1. calcium containing stones
  2. triple stones
  3. urate stones
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4
Q

effects of calculi

A
  1. urinary stasis (can be the cause of stones or caused by stones)
  2. ulceration (scratches the lining)
  3. bleeding
  4. infection (bacteria may be hiding in stone surface)
  5. pain
  6. fistula formation (stone can erode through organ)
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5
Q

what is acute tubular necrosis?

A

tubular epithelial cell death -> reduction/loss of tubular function

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5
Q

what is acute tubular necrosis?

A

tubular epithelial cell death -> reduction/loss of tubular function

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6
Q

what are the causes of acute tubular necrosis?

A

Ischaemic causes:
- shock
- haemorrhage
- major surgery
- severe burns
- dehydration

Toxic causes:
- endogenous products: myoglobin, haemoglobin
- drugs
- heavy metals
- organic solvents

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7
Q

tubular epithelial cells in ATN show varying degrees of:

A
  • swelling
  • vacuolation
  • flattening
  • sloughing
  • necrosis
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8
Q

what acute interstitial nephritis mainly caused by?

A

allergic reaction to drugs

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9
Q

what is acute pyelonephritis?

A

infection of the kidney, usually bacterial infection

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10
Q

bacteria may derive from (in acute pyelonephritis)?

A

-> ascending spread from bladder
predisposing factors include:
- lower urinary tract obstruction
- vesicoureteric reflux
- diabetes
- pregnancy
-> haematogenous spread (bacteraemia)

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11
Q

chronic pyelonephritis may be due to:

A

-> vesicoereteric REFLUX
-> OBSTRUCTION

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12
Q

what appearance does the kidney have in chronic pyelonephritis

A

flea-bitten appearance, cortex has collapsed

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13
Q

what mimics renal cell carcinoma?

A

xanthogranulomatous pyelonephritis

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14
Q

what differentiates xanthogranulomatous pyelonephritis from renal cell carcinoma?

A

presence of foam cells in xanthogranulomatous pyelonephritis

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15
Q

what are the complications of acute pyelonephritis?

A
  • septic shock
  • acute renal failure
  • pyonephrosis
  • perinephric abscess
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16
Q

what is hydronephrosis?

A

dilatation of renal pelvis and calyces filled with fluid with progressive kidney enlargement and parenchymal atrophy, eventually renal cortex is thinned out due to obstruction of urine outflow

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17
Q

microscopic changes in hydronephrosis

A
  • tubules and bowman’s spaces are dilated
  • tubular epithelium flattens
    eventually
  • tubular atrophy with fibrosis
  • glomeruli disappears
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18
Q

what is pyonephrosis

A

infected hydronephrosis with pus in the dilated calyces and pelvis

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19
Q

what is pyoureter

A

hydroureter infected and contains pus

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20
Q

what are the triad clinical features of renal cell carcinoma?

A

painless haematuria
mass in flank
fever

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21
Q

gross features of clear cell renal cell carcinoma?

A
  • unilateral, solitary, CIRCUMSCRIBED appearance
  • yellowish cut surface with variegated appearance due to necrosis and haemorrhage
  • possible invasion of renal vein
  • may metastasise
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22
Q

microscopic features of clear cell renal cell carcinoma?

A
  • polygonal cells with clear cytoplasm
  • delicate branching vasculature
  • invasion of renal vein
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23
Q

what is urothelial carcinoma of the kidney? (can affect ureter and bladder)

A
  • may be non-invasive papillary urothelial carcinoma or invasive carcinoma
  • involves the areas of the kidney lined by urothelium
  • pts are at very high risk of recurrent tumours anywhere in the urothelial tract
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24
Q

what is angiomyolipoma?

A
  • benign tumour of the kidney that can become very big
  • combination of fat cells, blood vessels and myoid spindle cells
  • may be sporadic or associated with tuberous sclerosis
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25
Q

gross and microscopic appearances of angiomyolipoma

A

GROSS
- unencapsulated
- yellow (fatty) areas

MICROSCOPIC
- mixture of myoid spindle cells, adipocytes and blood vessels
- myoid cells show immunostaining for HMB-45

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26
Q

how does benign prostate hyperplasia come about?

A
  • in the prostate, type 2 5alpha-reductase in the stromal cells converts testosterone to dihydrotestosterone (DHT)
  • DHT binds to androgen receptors in the epithelial and stromal cells and induces the production of growth factors that increase the growth of these cells
  • causes hyperplasia of the epithelial and stromal cells
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27
Q

where does benign prostate hyperplasia occur?

A

transitional zone -> compression of prostatic urethra -> partial obstruction (lower UTI obstruction)

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28
Q

complications of benign prostate hyperplasia

A
  1. bladder hypertrophy
  2. bladder distension and hypotonic
  3. bladder diverticulum
  4. UTI
  5. urolithiasis
  6. hydronephrosis and hydroureter
  7. chronic kidney disease
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29
Q

what is the most common type of prostatic carcinoma?

A

acinar adenocarcinoma

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30
Q

condyloma acuminatum is a benign tumour of the penis on coronal sulcus, inner surface of prepuce, what HPV type is it associated with?

A

HPV type 6 and 11

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31
Q

squamous cell carcinoma of the penis is associated with HPV types?

A

HPV type 16 and 18

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32
Q

testicular tumours are mainly

A

germ cell tumours

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33
Q

predisposing factors of testicular tumours

A
  1. crytorchidism (undescended testicle into scrotum)
  2. genetic factors
  3. testicular dysgenesis (abnormal organ development)
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34
Q

what are the differences between seminomatous and non-seminomatous germ cell tumours?

A

seminomas: (most common germ cell tumour)
- remain localised for a long time
- radiosensitive
- spread by lymphatics to para-aortic nodes

NSGCT:
- metastasise earlier
- radioresistant
- spread by haematogenous route

35
Q

yolk sac tumour is the most common testicular tumour in

A

infants

36
Q

teratoma is always __ in males

A

malignant
(can be benign or malignant in females)

37
Q

what are the treatment options for chronic renal failure?

A
  • haemodialysis
  • peritoneal dialysis
  • renal transplant
38
Q

pathology of chronic renal failure

A
  • end stage of many different types of glomerular disease
  • bilateral small contracted kidneys
  • widespread glomerulosclerosis, tubular atrophy, interstitial fibrosis
  • urine volume may be normal or polyuria as tubules cannot concentrate glomerular filtrate
  • terminal oliguria when no functioning nephrons left
39
Q

signs of acute renal failure

A
  • oliguria/anuria (decrease/absence in urine production)
  • azotaemia (increase of serum creatinine)
40
Q

pre-renal causes of acute renal failure

A
  • hypotension
  • haemorrhage
  • severe dehydration
  • shock
  • heart disease
  • liver failure
41
Q

renal causes of acute renal failure

A
  • glomerulonephritis
  • acute tubular necrosis
  • acute interstitial nephritis
  • haemolytic uraemic syndrome
  • vasculitis
  • infections (eg. pyelonephritis)
42
Q

post-renal causes of acute renal failure

A
  • acute urinary tract outlet obstruction
  • acute atonia, hypotonia of the bladder
42
Q

post-renal causes of acute renal failure

A
  • acute urinary tract outlet obstruction
  • acute atonia, hypotonia of the bladder
43
Q

nephrotic syndrome -
nephritic syndrome -
microscopic haematuria -
acute renal failure -
chronic renal failure -

A

nephrotic syndrome - leaky filters
nephritic syndrome - some glomeruli leaky, some unable to filter
microscopic haematuria - mild blood leak
acute renal failure - sudden development of inability to filter
chronic renal failure - slow development of inability to filter

44
Q

what modalities are involved in renal biopsy?

A

light microscopy: formalin
immunofluorescence: fresh (saline-moistened filter paper)
electron microscopy: glutaraldehyde

45
Q

what are the antibody-mediated mechanisms in glomerular injury?

A

1) in situ formation of Ag-Ab formation
- against native antigen (attacking an antigen part of the glomerular structure)
- against planted antigen that localised in the glomerulus

2) circulating immune complexes

3) antineutrophil cytoplasmic antibodies

46
Q

Goodpasture’s syndrome is an autoimmune disease in which the antibodies attack the _________ in ________ and ________

A

basement membrane; lungs and kidney
(glomerulus BM and alveoli BM are made up of the same type IV collagen)

47
Q

Goodpasture’s syndrome can lead to ___ in the kidney

A

crescentic glomerulonephritis

48
Q

what is amyloidosis?

A

amyloidosis is extracellular accumulation of fibrillary proteins

49
Q

for amyloidosis diagnosis, the extracellular accumulation of fibrillary proteins should show both:

A
  1. positive staining with Congo red stain
  2. apple green birefringence under polarised light
50
Q

amyloidosis usually occurs in kidney patients that have:

A
  • plasma cell dyscrasia
  • chronic inflammatory diseases or neoplasms
51
Q

what does the proteins in amyloidosis form?

A

antiparallel beta-pleated sheets

52
Q

what is the commonest cause of glomerulonephritis?

A

IgA nephropathy

52
Q

what is the commonest cause of glomerulonephritis?

A

IgA nephropathy

53
Q

what is the commonest cause of end stage renal disease?

A

diabetic nephropathy

54
Q

Diabetic nephropathy is the ______ of collagen, forming _______

A

glycosylation; advanced glycation end products

55
Q

effect of diabetic nephropathy on the kidneys

A

glomeruli:
- glomerular basement membrane thickening
- mesangial widening -> forms kimmelsteil-wilson nodules

tubules:
- thickened BM
- tubular atrophy

interstitium:
- fibrosis

vessels:
- arteriolar hyalinosis
- arteriosclerosis

56
Q

likely causes of renal infarction (wedge-shaped)

A
  • thromboembolism (#1 cause)
  • atherosclerosis
  • malignant hypertension
  • renal vein occlusion
  • hypovolemic shock
57
Q

2 clinical manifestations of renal infarction

A
  1. acute flank pain
  2. haematuria
58
Q

What is seen IgA glomerulonephritis?

A

microscopic proteinuria with haematuria

59
Q

what conditions will cause nephritic syndrome?

A
  • post-infectious glomerulonephritis (post streptococci)
  • membranoproliferative glomerulonephritis
60
Q

membranoproliferative glomerulonephritis is associated with decreased serum ___

A

C3

61
Q

what are the changes in EM seen in minimal change disease?

A

fusion of foot processes and occasional detachment from basement membrane

62
Q

focal segmental glomerulosclerosis is due to ___

A

podocyte injury with loss of podocytes

63
Q

what is the commonest cause of childhood nephrotic syndrome?

A

minimal change disease

64
Q

are there any changes observed in light microscopy and/or immunofluorescence test in minimal change disease?

A

no

65
Q

what are the changes seen in LM and IF in focal segmental glomerulosclerosis?

A

LM: some glomeruli show segmental sclerosis
IF: sclerotic lesions stain with IgM and C3

66
Q

what is the commonest cause of nephrotic syndrome in adults?

A

membranous glomerulopathy

67
Q

what are the changes seen in LM and IF in membranous glomerulopathy?

A

LM: basement membrane thickening
IF: IgG and C3 on the epi-membranous side of BM forming string of pearl appearance

68
Q

what are the immune complex deposits present in lupus nephritis?

A

IgG, IgA, IgM, C1q (dominant), C3

69
Q

what is seen in hypertensive nephrosclerosis?

A

arteriolar hyalinosis
arteriosclerosis

70
Q

what kind of urine will patient complain of in nephrotic syndrome?

A

frothy urine

71
Q

diseases causing nephrotic syndrome

A

common causes:
- minimal change disease (children)
- focal segmented glomerulosclerosis
- membranous glomerulopathy

uncommon causes:
- membranoproliferative glomerulonephritis
- IgA nephropathy

72
Q

Bacteraemia in UTI patient indicates

A

upper UTI

73
Q

what are the likely pathogens for UTIs

A

E coli
Staphylococcus saprophyticus

74
Q

Common pathogens and classical presentations of STDs:

A

ulcer:
- syphilis (treponema pallidum)
- haemophilus ducreyi
- hsv 2

discharge:
- neisseria gonorrhoea -> think, purulent discharge
- chlamydia trachomatis -> thinner, more fluid discharge
- trichomonas vaginalis -> frothy yellow green, purulent discharge

warts:
- HPV 6, 11 (condylomata acuminatum)

75
Q

Patients with urothelial carcinoma (invasive/non-invasive) are at risk of

A

recurrent urothelial tumours anywhere in the urothelial tract

76
Q

What are the two common pathology of the prostate gland?

A

BPH
Prostatic carcinoma

77
Q

Which zone of the prostate does these diseases commonly occur at?

A

BPH: TRANSITIONAL zone
prostatic carcinoma: PERIPHERAL zone

78
Q

Unlike those in the ovary, epithelial tumours in the testicles are very

A

uncommon

79
Q

clinical symptoms of BPH

A
  • hesitancy, urgency
  • nocturia
  • poor urinary stream
80
Q

what is a distinct feature of condyloma acuminatum?

A

clear vacuolation

81
Q

what is raised in a patient with BPH?

A

Prostate Specific Antigen

82
Q

what tumour marker is raised in yolk sac tumour of the testis?

A

alpha fetoprotein

83
Q

what is the diagnostic criteria for ESRD?

A

GFR is <5% of normal

84
Q

3 likely causes of ESRD

A
  • diabetic nephropathy
  • glomerulonephritis
  • hypertension