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Surgery > Urology > Flashcards

Urology Flashcards

1
Q

Classify testicular tumours and which is most common

A

Germ cell (MC; 95%)
Sex cord stromal
Spermatic cord/paratesticular
Lymphoma

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2
Q

What is the MC type of testicular germ cell tumour

A

Seminoma = malignant proliferation of spermatogonia

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3
Q

Contrast seminomatous and non-seminomatous testicular cancers

A

Seminoma:
- 40-50yo
- respond well to radiotherapy (metabolically active & single cell line)
- slow growth and late metastasis
- good prognosis
- uniform mass without necrosis/haemorrhage

Non-seminoma
- aggressive and early metastasis
- most are mixed cell lines/tissue types
variable prognosis and response to radiotherapy depending on worst component

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4
Q

What do testicular germ cell tumours arise from

A

Germinal epithelium of seminiferous tubules

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5
Q

Discuss the evolution of germ cell tumours/precursor lesions

A

In situ germ cell neoplasia (IGCN)
–> seminoma, or
–> embryonal carcinoma –> teratoma, choriocarcinoma, yolk sac tumour

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6
Q

What are the clinical features of testicular neoplasms

A

Possible early dragging sensation
Small firm lump in testis (usually painless but may have dull pain in testes/lower abdomen)
Metastatic features
- Haematogenous –> lungs (dyspnoea, haemoptysis), brain (seizures, headache, vomiting, nausea)
- Lymphatic –> retroperitoneal LNs (lower back pain)

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7
Q

Epidemiology for testicular germ cell tumours

A

Caucasian, 15-35yo, rising incidence

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8
Q

Risk factors for testicular germ cell tumours

A

Cryptorchidism
Klinefelter syndrome (XXY)
Hypospadia
Isochrome p12 abnormality
Evironment

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9
Q

What is an embryonal carcinoma and it’s features

A

Malignant tumour comprised of immature cells resembling early embryo with peak incidence in 20s-30s

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10
Q

What hormone/marker is high in embryonal carcinoma

A

High hCG

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11
Q

What is a testicular choriocarcinoma and it’s behaviour

A

Highly malignant proliferation of cytotrophoblastic and syncytiotrophoblastic cells that has early, aggressive haemorrhagic metastases to brain and lungs

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12
Q

What is the tumour marker for choriocarcinoma and the clinical consequences of this

A

Very very high hCG: the alpha sub-unit is similar to that of FSH and LH producing gynaecomastia and similar to TSH producing hyperthyroidism

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13
Q

What is an endodermal sinus tumour and it’s features

A

Malignant proliferation of yolk sac cells most common in children with a prepubertal type affecting <3yos and a post-pubertal type that has a mixed pattern and worse prognosis

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14
Q

What histology is characteristic of yolk sac tumour

A

Schiller-Duval bodies (glomerulus like)

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15
Q

What tumour marker is associated with yolk-sac tumours

A

AFP

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16
Q

What is a teratoma and the features of it’s subtypes

A

Tumour composed of mature/immature foetal tissue derived from at least 2 embryonic germ cell layers (ectoderm/mesoderm/endoderm) resulting in a large heterogenous mass with solid, cartilaginous, and cystic areas

Mature
- prepubertal form MC = benign
- postpubertal = malignant

Immature
- postpuberal = malignant

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17
Q

What are the main testicular sex cord stromal tumours

A

Leydig cell tumour
Sertoli cell tumour

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18
Q

Where do testicular sertoli cell tumours originate and what are their features

A

Inside seminiferous tubules
90% benign and hormonally inactive
Arranged in trabeculae and cords

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19
Q

Where do testicular leydig cell tumours originate and what are their features

A

Outside seminiferous tubules
90% benign but hormonally active
- MC = testosterone resulting in precocious male puberty, testicular swelling
- oestrogen results in delayed male puberty, feminisation

Reinke crystals

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20
Q

Who does testicular B cell lymphoma affect and what is it’s behaviour

A

MC testicular ca in males > 60yo
Very malignant

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21
Q

What are examples of paratesticular/spermatic cord tumours

A

Embryonal rhabdomyoma
Lipoma
Lipsarcoma
Adenomatoid

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22
Q

What extragonadal sites to germ cell tumours rarely occur in

A

Midline from pituitary
Mediastinum
Retroperitoneum

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23
Q

Where to testicular tumours metastasise to (vs scrotal LNs)

A

Para-aortal (vs superficial inguinal) LNs

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24
Q

How is a testicular tumour diagnosed

A

Clinical features and -ve transillumination

USS of testicle
Assay of serum tumour markers: PALP, hCG, AFP, LDH
CT/MRI for metastasis

Do not biopsy as a scrotal incision provides another pathway for LN mets. Instead Dx is confirmed histologically post-orchidectomy.

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25
Q

What testicular marker is associated with seminomas

A

LDH and PALP

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26
Q

Seminoma Mx

A

Orchidectomy via inguinal approach to avoid spillage of highly metastatic tumour in scrotum

Adjuvant therapy with chemo/radiotherapy to para-aortic LNs is preferred (carboplatin)
Alternative: intensive surveillance –> Tx if relapse

Metastatic disease: combination chemo

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27
Q

Non-seminoma Mx

A

Orchidectomy via inguinal approach to avoid spillage of highly metastatic tumour in scrotum

Moderate-high risk: adjuvant combination chemo therapy (uncommon alternative = retroperitoneal LN dissection)

Relapse from initial chemo: further cisplatin and ifosfamide chemo or high-dose carboplatin chemo and etoposide and stem cell transplant

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28
Q

Do males retain fertility after testicular chemo

A

Mostly

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29
Q

What is a varicocoele

A

Abnormal enlargement and tortuosity of pampiniform venous plexus in scrotum

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30
Q

Varicocoele aetiology

A

Increased venous pressure of spermatic vein (testicular vein)

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31
Q

What side does varicocoele usually occur on and why

A

Left

Right spermatic vein drains directly to IVC
Left spermatic vein is longer, has no valves and inserts at a right angle into L renal vein resulting in slower drainage and increased back pressure

Consider RCC compressing L renal vein in a patient with L varicocoele

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32
Q

What is a secondary cause of varicocoele

A

Retroperitoneal mass/thrombotic occlusion in plexus –> obstructed venous drainage

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33
Q

How does varicocele present

A

Scrotal swelling
Painless/dull ache/heavy feeling
“Bag of worms” appearance/feeling on palpation
Sx may worsen when standing or with valsalva
Increased temp –> infertility

-ve transillumination

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34
Q

Dx of varicocoele

A

Clinical Dx

Confirm with scrotal USS with colour Doppler

If a varicocele does not diminish in supine position, or in a R sided varicocoele, consider further imaging to rule out retroperitoneal mass –> usually CT/MRI abdomen

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35
Q

Mx of varicocoele

A

Reassurance
Observation
Consider surgical options:
- laparoscopic ligation of L renal vein (collaterals will form
- percutaneous embolisation

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36
Q

What is a hydrocoele

A

Fluid accumulation within cavity bound by tunica vaginalis of scrotum

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37
Q

Aetiology

A

MC = inflow presenting in infancy: patent tunica vaginalis = communication w/ peritoneal cavity
Outflow presenting in older patients: trauma/infection of lymphatics –> unable to remove fluid produced by tunica vaginalis (or overproduction of this fluid)

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38
Q

Clinical features of hydrocoele

A

Fluctuant painless scrotal swelling
Can palpate above
+ve transillumination
Size changes during day (increased intra-abdominal pressure e.g., with coughing, straining, crying, raising arms increases flow of peritoneal fluid into scrotal sac)
Can be complicated by haematocoele

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39
Q

Dx of hydrocoele

A

Clinical picture
Confirmed by scrotal USS

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40
Q

Mx of hydrocoele

A

Observation: many hydroceles resolve before the age of 2 years

Elective surgical repair is indicated for persistence of a hydrocele beyond 2 years of age to avoid complications such as incarcerated inguinal hernia.
- Complete excision of tunica vaginalis is appropriate treatment
- Aspiration can be done in older patients but can recur

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41
Q

What is Testicular Torsion

A

Twisting of spermatic cord, obstructing venous drainage of testes –> vascular engorgement and haemorrhagic infarct

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42
Q

What is the aetiology of testicular torsion

A

Neonatal: idiopathic
Children/adolescents: processus vaginalis seals too high above testis –> increased mobility esp. ~12-16yo as volume increases

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43
Q

Diagnosis of testicular torsion

A

Clinical presentation

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44
Q

Clinical presentation of testicular torsion

A

Sudden severe testicular/lower abdominal pain 2˚ ischaemia

Swelling
Testes sit higher and horizontally

Absent cremasteric reflex

Irreversible damage and redness after ~6 hours

Death and black discolouration ~ 12 hours

45
Q

Treatment for testicular torsion

A
  1. Immediate urological surgical consultation
  2. IV access, NPO, morphine and ondansetron
  3. < 6 hours and viable testis: orchidopexy vs late and non-viable: orchidectomy +/- prosthetic
46
Q

DDx for testicular torsion

A

Torsion of Hydatid of Morgani = cystic remnant of Mullerian duct
Same Sx as testicular lesion but no functional consequence

47
Q

What sign is pathognomic for torsion of hydatid of morgani and how is it Dx

A

Blue dot sign (infarction of the hydatid of Morgagni that appears blue through the scrotal skin)

Scrotal USS with colour Doppler

48
Q

What is an epididymal cyst

A

Cystic collection of sperm within epididymal duct due to increased back pressure of sperm from trauma/infection presenting as fluctuant swelling of upper testicular pole palpable as distinct from testes and +vely transilluminableC

49
Q

What are DDx for scrotal mass

A

Hydrocoele
Varicocoele
Epididymal cyst
Epidymitis/orchitis
Tumour

50
Q

Complications, Dx and Tx of epididymal cyst

A

Rupture: sperm exposed to immune components –> granuloma

Dx: clinical and USS
Mx: surgical spermatocoelectomy

51
Q

DDx of haematuria

A

Glomerular haematuria:

  • Nephritic syndrome (characteristic of glomerulonephritis) → haematuria with proteinuria is considered GN until proven otherwise
  • Isolated haematuria:
    • Transient e.g. strenuous exercise, infectio
    • Persistent e.g. IgA nephropathy, Alport syndrome, thin basement membrane nephropathy

Non-glomerular haematuria:

  • Urolithiasis Infection → cystitis, urethritis, prostatitis
  • Malignancy → Urothelial ca, renal cell ca, prostate ca, Wilms tumour (children)
  • Coagulation disorders → platelet dysfunction, haemophilia
  • Urinary tract obstruction → BPH, congenital anomalies
  • Polycystic kidney disease
  • Renal papillary necrosis → sickle cell disease, acute pyelonephritis, diabetes, analgesics
  • Trauma → urethral, bladder, ureteral or renal injury
  • Drugs – warfarin, heparin, sulfonamides
52
Q

Classifications of haematuria

A

Macroscopic (gross): frank blood in urine resulting in visible red/brown urine discolouration

Microscopic: >3 RBCs per high-power field on urinary microscopy but no urine discolouration

  • Urine dipstick analysis not sufficient to Dx microscopic → requires urine microscopy

Consider malignancy in painless haematuria → painful indicative of more infective/inflammatory cause

53
Q

How does red cell morphology provide information about location of haematuria

A
  • Isomorphic (normal) RBCs (and presence of blood clots): LUT origin
  • Dysmorphic RBCs/fragmented shards: glomerular origin (RBCs pass through damaged glomeruli subjected to severe osmotic stress inside renal tubules → morphological changes)
54
Q

In a positive urine dipstick for red cells what are non-haematuria differentials

A
  • Isomorphic (normal) RBCs (and presence of blood clots): LUT origin
  • Dysmorphic RBCs/fragmented shards: glomerular origin (RBCs pass through damaged glomeruli subjected to severe osmotic stress inside renal tubules → morphological changes)
55
Q

How should a patient with haematuria be examined

A
  • BP assessment (elevated BP in patients with glomerulopathic causes of haematuria)
  • Systemic features of infection (abnormal vitals, dehydration)
  • GIT, cardiovascular, respiratory, and genitourinary examinations
  • Renal angle or flank tenderness may indicate renal colic
  • Presence of ascites/peripheral edema (earliest sign = periorbital edema pedal, sacral, abdomen, lung)
  • Examination of external genitalia if urethral injury/trauma
56
Q

How should a patient with haematuria be investigated

A

STANDARD

MSU (2 consecutive MSU samples optimum for diagnosis)
- UA and MC&S to exclude infection
- Random urine PCR or dipstick for protein (e.g., nephrotic syndrome/renal disease)
- All patients with macroscopic haematuria and patients with microscopic haematuria and risk factors for RCC (smoking, compound analgesic use, industrial toxin exposure, age > 50 years) should have urine cytology

Bloods: UEC with eGFR

ISOLATED MICRO HAEMATURIA: no cancer risk factors, no proteinuria and normal GFR –> observe and review

MICRO HAEMATURIA AND PROTEINURIA/REDUCED GFR: renal USS and nephrology review +/- renal biopsy

MICRO HAEMATURIA AND CA RISK FACTOR: renal USS/CT IVP and urology review

MACRO HAEMATURIA: CT IVP or rena tract USS and refer to urology

57
Q

What is Benign Prostatic Hyperplasia?

A

Hyperplasia of prostatic stroma and glands occurring in the transitional zone of the prostate

58
Q

Pathophysiology of BPH

A

5a reductase activity increases with age –> increased conversion of testosterone to dihydrotestosterone –> DHT acts on androgen receptor of stromal and epithelial cells to prevent apoptosis of cells –> periurethral hyperplastic nodules –> stretching/compression/distortion of urethra and BOO

59
Q

Epidemiology of BPH

A

Males > 60yo

60
Q

Symptoms of BPH

A

Obstructive LUTS: hesitancy, straining, poor/intermittent stream, terminal driblling, sensation of incomplete voiding, overflow incontinence

Irritative LUTS (detrusor hyperactivity): frequency, urgency, urge incontinence, nocturia, occasionally dysuria

Occassional severe haematuria from rupture of prostatic veins or due to bacteruria or stone disease

61
Q

Complications of BPH

A

UTI
Hydronephrosis and impaired real Fx
Bladder diverticula

62
Q

Ex of BPH pts

A

Abdominal exam for bladder enlargement and percussion for retention

DRE: symmetrically enlarged, smooth, firm, non-tender prostate with rubbery/elastic texture and poorly defined median sulcus

63
Q

Ix for BPH pt

A

International Prostate Symptom Score to define severity of Sx

Urine MC&S

PSA (prostate specific antigen; above expected for age consider prostatitis or prostate cancer)
UEC and eGFR

USS (abdominal or transrectal to assess volume and morphology)
Consider uroflowmetry and other imaging e.g., CT/MRI before surgery
Cystoscopy to assess bladder if pathology suspected

64
Q

Mx of BPH

A

Mild-moderate Sx: lifestyle changes alone due to risk of worsening Sx with Tx

Moderate-severe:
- alpha-blocker e.g., tamsulosin –> relaxes bladder neck SM tone
- 5a reductase inhibitor e.g., inhibitor e.g., dutaseride/finasteride –> blocks conversion of testosterone to DHT to minimise prostatic growth and enlargement
- Surgical: laser therapy, trans-urethral needle ablation, trans-urethral resection of prostate, open prostatectomy

65
Q

When is surgery for BPH indicated

A

Deterioration in renal Fx or development of upper tract dilatation

66
Q

How should acute retention in BPH be managed

A

Relieve pain, catheterise and drain bladder (suprapubic if ureteral catheterisation not possible)

67
Q

SEs of alpha adrenergic antagonists used in bPH

A

Retrograde ejaculation
Erectile dysfunction
Hypotension
Tachycardia
Dizziness
Nasal congestion

68
Q

SEs of 5a reductase inhibitors for BPH

A

Erectile dysfunction
Reduced libido
Reduced ejaculate and sperm count

69
Q

SE of endoscopic TURP

A

Urinary incontinence
Erectile dysfunction

70
Q

What is prostate adenocarcinoma

A

Malignant proliferation of prostatic glands usually in posterior peripheral zone of prostate

71
Q

Epidemiology of prostate cancer

A

MCC of cancer in men
2nd MCC of cancer-related death
Common with increasing age
By 80yo 80% of men have malignant foci within the gland

72
Q

Risk factors for prostate cancer

A

Advancing age
Race (black)
FHx
Genes e.g., BRCA2

73
Q

Clinical features prostate cancer

A

Usually only produces LUTS Sx at late stage due to posterior location

Metastatic: lower back, hip and skeletal pain, weight loss, anaemia

DRE: nodule hard prostate/irregular gland/palpable lump

74
Q

Where does prostate cancer metastasise to

A

Axial skeletal via vertebral venous plexus
Osteoblastic (not lytic) lesions
Produces hip and lower back pain

75
Q

How is prostate cancer Ix and Dx

A

Serum PSA
- PSA level above median for age group –> higher risk for aggressive prostate cancer
- PSA > 4-10ng/ml = abnormal but can be due to BPH or cancer
- PSA > 10ng/ml = cancer in > 50% of cases
- PSA > 16ng/ml = suggests metastatic disease

TRUS and extended sampling prostatic biopsy
- Use Gleason score of histological appearance

Endorectal coil MRI to detect extraprostatic extension
Pelvic MRI with dynamic contrast to assess extent of disease

Renal USS for evidence of dilatation
XR/isotopic bone scan: osteosclerotic mets

76
Q

Mx of prostatic carcinoma

A

Gleason score of 6 or below and localised prostate cancer: watchful waiting with regular PSA and prostatic biopsies –> more aggresive change –> Tx

Localised to prostate: radical prostatectomy, external beam radiotherapy, or brachytherapy (incontinence and sexual dysfunction)
- radiotherapy MC in older pts to avoid surgery

Locally advanced prostate cancer without distant mets: combined androgen deprivation and radiotherapy
- GnRH agonist e.g., goserelin (NB. produces rise in LH –> tumour flare if metastatic so combine with antiandrogen e.g., flutamide initially)
- Orchidectomy
- Andrgen R blockers e.g., bicalutamide
- Androgen synthesis inhibitor

If considering androgen deprivation Tx: FBC, UEC, LFTs, testosterone

Metastatic prostate cancer:
- Androgen deprivation to achieve castration: successful palliation for ~2yrs
- Castration resistant –> corticosteroids/oestrogens/chemo e.g., docetaxel

77
Q

Renal cell carcinomas arise from

A

Proximal tubular epithelial ells

78
Q

RCC epidemiology

A

> 50yo
M > F

79
Q

Clinical features of RCCs

A

Often asymptomatic incidental finding

Haematuria (pelvicalyceal invasion)
Loin pain (late; tumour stretches capsule)
Mass in flank
L sided varicocoele (if invasion of renal vein and obstructed drainage of L testicular vein)

Malaise
Anorexia
Weight loss
1/3 present as mets: bone pain, path #, cannon-ball deposits in lung, cerebral Sx

Paraneoplastic:
- EPO/depressed EPO: Polycythaemia/anaemia
- Renin: HTN
- PTHrP: Hypercalcaaemia
- ACTH: Cushing
- Cytokines: pyrexia

80
Q

Diagnosis of RCC

A

FBC, UEC, CMP, ESR, LFTs (may be abnormal)

USS may demonstrate solid lesion

CT to ID renal lesion and involvement of renal veins/IVC

MRI best for tumour staging

81
Q

Risk factors for RCC

A

Von Hippel Lindau Syndrome
Smoking
Obesity
Occupational exposures
Chemotherapy in childhood

82
Q

Mx RCC

A

Nephrectomy unless bilateral tumours or contralateral kidney Fx is poor –> partial nephrectomy

Metastasis:
- Nephrectomy can result in regression of mets
- Tyrosine kinase inhibitors e.g., sunitinib or immunotherapy e.g., high dose IL2
- Possible excision of isolated mets

83
Q

How does RCC spread

A

Local expansion into renal capsule
-> into perinephric fat and hilum –> para-aortic nodes
-> into renal sinus and IVC

–> CNS, lungs, bone

84
Q

Is urine cytology helpful in Dx of RCC

A

Nope

85
Q

What tumours metastasise to bone

A

Prostate
Thyroid
Breast
Liver
Kidney

86
Q

What is urothelial carcinoma derived from and where does it occur

A

Transitional cell epithelium lining calyces, renal pelvis, ureter, bladder, urethra

87
Q

Urothelial carcinoma epidemiology

A

M&raquo_space;> F
> 40yo

88
Q

Risk factors for urothelial carcinoma

A

Cigarette smoking

Exposure to industrial carcinogens e.g., in rubber industry: azo dye, heavy meals, phenacetin, aromatic amines like benzidine and aniline dyes
Iatrogenic e.g., pelvic irradiation, cyclophosphamide, phenacetin

Chronic inflammation e.g., schistosomiasis, chronic nephrolithiasis, recurrent UTI

89
Q

Clinical features of urothelial carcinoma

A

Painless frank haematuria = MC
- possible pain if clot retention

Irritative voiding Sx: dysuria, urinary frequency, urgency (but no bacteruria/sterile cultures)

Infiltration of adjacent nerves: suprapubic/perineal/rectal pain

BOO if tumour/blood clot at bladder neck

Flank pain if ureteric obstruction

90
Q

Investigations for urothelial carcinoma

A
  1. Urine analysis (RBCs, possible pyuria)
  2. Urine cytology for malignant cells
  3. Urinary tumour markers
  4. Cystoscopy to assess tumour burden and for biopsy
  5. CT/MRI of pelvis
  6. Consider bone scan if Sx or elevated ALP and CXR if invasive disease
91
Q

Management of urothelial bladder carcinoma

A

Superficial bladder TCCs within BM: transurethral resection or local diathermy
- Follow up cystoscopy and urine cytology

Recurrent superficial TCC: bladder instillation of BCG or with chemo (e.g., mitomycin)

Muscle-invasive < 70yo: neoadjuvant cisplatin based chemo, radical cystectomy –> new bladder made from SB joined to urethra or ileal conduit
- Alt: bladder preservation with cisplatin and 5FU chemoradiotherapy and transurethral resection

Muscle-invasive 70yo+: neoadjuvant cisplatin based chemo, radical radiotherapy + salvage cystectomy if recurrent

Metastatic: cisplatin based chemo

92
Q

Bladder outflow obstruction = lower urinary tract obstruction

A

Bladder obstruction
- Bladder carcinoma
- Bladder calculi
- Blood clot
- Neurogenic bladder (detrusor underactivity from DM, MS, sacral nerve injury etc., or sphincter overactivity e.g., spinal cord injury/tumours)
- Congenital bladder neck obstruction
Urethral obstruction
- Prostatic enlargement (BPH/Ca)
- Congenital: posterior urethral valves
- Stricture (calculus, gonococcal, after instrumentation)
- Urolithiasis
- Meatal stenosis
Mechanical obstruction
- Kinked/plugged indwelling catheter
Extrinsic compression
- Tumours: CRC, cervical, retroperitoneal
- Diverticulitis, AA, retroperitoneal fibrosis
- Phimosis
- Pregnancy

93
Q

Describe the classifications of neurogenic bladder

A

Spastic (UMN) → detrusor-sphincter dyssynergia
- The bladder contracts against a closed urethral sphincter due to a loss of coordination between the central (pontine) and peripheral (sacral) micturition centers. Seen in spinal lesions at/above T12 (traumatic spinal cord injuries, multiple sclerosis). Patients may present with urinary retention or urge incontinence (due to recurrent detrusor contractions).
- Flaccid (LMN) → detrusor-arreflexia but intact urethral sphincter innervation
- Due to a spinal cord lesion/s at S2 or between S2–S4 or due to peripheral nerve damage. Since sympathetic control of urethral tone is above the level of the lesion. (i.e., at T12–L2), the urethral function is preserved, causing a functional BOO/urinary retention.

94
Q

Pathophysiology of Chronic BOO

A
  1. Urine continues to be formed despite obstruction to flow
  2. Progressive rise in intraluminal pressure and dilatation proximal to site of obstruction
    - dilatation of renal pelvis and/or ureter = hydronephrosis and hydroureter
  3. Compression and thinning of renal parenchyma –> renal atrophy
95
Q

Pathophysiology of Acute BOO

A
  1. Acute BOO –> transient arterial vasodilation –> vasoconstriction likely mediated by angiotensin and thromboxane A2
  2. Ischaemic interstitial damage mediated by free ROS and inflammatory cytokines compounds damage induced by compression of renal parenchyma
96
Q

Clinical features of BOO

A

Obstructive LUTS: hesitancy, poor/intermittent stream, double voiding, sensation of incomplete voiding, overflow incontinence, terminal dribbling
Irritative LUTS: nocturia, frequency, urge, urge incontinence
Suprapubic pain

Urinary retention, palpable distended bladder
Complete anuria suggests complete bilateral obstruction or complete obstruction of a single kidney

Untreated: progressive renal failure
UTI Sx
Hydronephrosis: palpable kidney

NB. Ex of genitalia, rectum, or vagina is performed since prostatic obstruction and pelvic malignancy are common causes of UTO

97
Q

Ix of obstructive uropathy

A

UA dipstick +/- MC&S

FBC, UEC and eGFR

Renal USS (? hydronephrosis)

Non-contrast CT pyelogram (? calculi)

IV pyelogram: delayed nephrogram and drainage if obstruction present
- CI if renal impairment or contrast allergy

CT scan abdo and pelvis if hydronephrosis of unknown cause

Voiding cystourethrogram (child with hydronephrosis ? PUVs/ureterocoele + shows VUR)

98
Q

Complications of BOO

A

Cystitis, pyelonephritis, perinephric abscess
Obstructive nephropathy (renal impairment from UTO)
Nephrolithiasis (stasis of urine predisposes patients to calculi formation within the urinary tract)
Bladder trabeculation and pseudodiverticula formation
AKI
Hydronephrosis and loss of renal function

99
Q

Mx BOO

A

Obstructed, infected urinary tract = medical emergency –> septicaemia
- Bladder catheterisation for rapid relief of outflow tract (suprapubic if cannot place urethral)
- Obstructed and hydronephrotic kidneys can be relieved by percutaneous nephrostomy under USS guidance
- Obstructed ureters can be relieved by cystoscopic stenting

Partial obstruction is not an emergency
- Calculi: trial passage with analgesia, rehydration +/- alpha blockers if < 10mm or remove/stent/nephrostomy if 10mm+
- Non-calculi obstruction: ureteric stent or nephrostomy or as per cause of obstruction

100
Q

Types of renal stones and MC type

A

Calcium oxalate (MC)
Calcium phosphate
Magnesium ammonium phosphate/struvite/mixed infective
Uric acid
Cystine

101
Q

Risks associated with renal stone disease

A

Bone disease
ESKD
HTN
MI

102
Q

Causes of renal tract stones

A
  • Dehydration
  • Hypercalaemia (hyperparathyroidism, malignancy, sarcoidosis, vit D ingestion)
  • Hypercalciuria (idiopathic, hypercalcaemia, high dietary calcium intake, excessive resorption from skeleton e.g., in immobilisation)
  • Hyperoxaluria (inborn error of metabolism, spinach/rhubarb/tea, dietary restriction of calcium, Crohn’s/ileal resection)
  • Hyperuricaemia and hyperuricosuria (TLS, myeloproliferative disorders, assoc. with gout)
  • UTI (proteus miribalis)
  • Cystinuria
  • Primary renal disease (PCKD, MSD, RTA)
  • Drugs (loop diuretics, antacids, glucocorticoids, vitD and C, acetazalomide)
103
Q

Which renal calculi are staghorn calculi are why

A

Magnesium ammonium phosphate stones as they form a cast of collecting system

104
Q

What organisms are associated with infective renal stones

A

Organisms that hydrolyse urea and form ammonium hydroxide e.g., proteus miribalis
- ammonium ion availability and alkalinity of urine favours stone formation

105
Q

Clinical features of urinary tract calculi

A

MC: pain –> sharp/dull/constant/intermittent/colicky
- if obstruction: fluids/diuretics may exacerbate pain
- exertion can exacaberate pain/haematuria if stones move

Ureteric colic: stone enters ureters and causes obstruction or spasm
- flank pain radiating to iliac fossa/testis/labia (distribution of L1 nerve root)
- assoc. w/ pallor, sweating, vomiting
- restless pt

Haematuria

Possibly features of UTI if concomitant infection

Bladder stones: bacteriuria, frequency, dysuria, haematuria
- Trigonitis –> perineal/introital pain
- BOO –> anuria and painful bladder distension

106
Q

Investigations for urinary tract calculi

A

Urine dipstick
MSU for MC&S
Urine bHCG (before CT)

Serum FBC, UEC, eGFR, calcium

USS: kidney stones, renal pelvis dilatation, may miss ureteric stones
- can be 1st line in young patients to avoid radiation
CT-KUB = best Dx test
- normal CT excludes calculous disease

Once passed: chemical analysis of stones

107
Q

Mx of urinary tract stones

A
  1. Analgesia e.g., NSAIDs (ibuprofen 400mg PO)/opioid
  2. Stones of < 0.5cm: usually pass spontaneously esp. if hydration maintained (aim for > 2.5L intake)
  3. Stone > 1cm: surgical/radiological intervention
    - Extracorporeal shockwave lithotripsy to fragment stones –> pass spontaneously
    - Ureteroscopy with YAG laser for larger stones
    - Percutaneous nephrolithotomy
108
Q

Which renal calculi are radiolucent

A

Uric acid stones (can be seen on CT or otherwise as a filling defect with contrast)
Mixed infective stones are barely radio-opaque

Surgery (17 decks)

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