Genitourinary Flashcards

1
Q

What is the most common zone of the prostate that carcinomas occur?

A

4 zones of the prostate

  • i) Transitional zone 

  • ii) Central zone 

  • iii) Peripheral zone 

  • iv) Anterior fibromuscular stroma 


Clinical important of zones of prostate

  • Transitional zone surrounds the urethra and is the part of the prostate predominately affected by nodular hyperplasia. Only 20% of prostate carcinomas occur here 

  • Peripheral zone is palpable on rectal examination. 75% of prostate carcinomas occur here
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2
Q

Incidence of prostate cancer

A
  • Most common cancer in Australian men, lifetime risk is 1/6
  • Often occurs in men after the age of 50
  • More prevalent in African men and less prevalent in oriental men
  • Most commonly does not require care. Despite this prostate cancer remains the second biggest cause of male cancer death with 1/30 men dying from prostate cancer
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3
Q

Clinical features of prostate cancer

A

Early disease – asymptomatic

  • Patients who present with LUTS usually have an enlarged prostate secondary to BPH though prostate cancer may co-exist

Advanced disease

  1. Locally advanced disease - urinary symptoms similar to those in BPH e.g. frequency, nocturia, hesitancy, poor stream, dysuria. Haematuria may be present
  2. Metastatic disease - bone pain, fractures, cord compression
  3. Generalised symptoms of malignancy - anaemia, weight loss, depression
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4
Q

Diagnostic tests for prostate cancer

A
  1. Digital rectal examination (DRE) – firm nodule (T2) hard, craggy prostate (T3/4)
  2. PSA test
  • PSA rises with age so should be compared to norm for that age group
    1. Trans-rectal U/S biopsy (TRUS biopsy) - Diagnostic.
  • Complications:
    • Infection – all patients get prophylactic antibiotics but infection still occurs
    • Bleeding – patients may see blood PR, have haematuria or haematospermia which may last several weeks. Serious post-biopsy bleeding can occur. _Anti-coagulating drugs must be stopped befor_e a TRUS biopsy
    • Urinary retention
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5
Q

What is the grading score for prostate biopsy called and what type of cancer is the most common on histopathology

A
  • Prostate biopsy – Gleason score is used for grading prostate cancer
  • It gives prognostic information and indicator of tumour aggression
  • Histological grading system: 1-5
  • 95% of tumours are adenocarcinoma
  • Gleason sum score = most common tumour pattern histologically + worst pattern in a core biopsy e.g. 3+4 = 7
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6
Q

What are the treatment options for prostate cancer

A
  1. Radical prostatectomy
  • Indication: localized prostate cancer
  • Urinary catheter is left in-situ for 10 days post-operatively and not to be removed as re-insertion may disrupt urethral anastomosis
  • Complications:
    • Impotence, incontinence, recurrence of disease, mortality
  1. Radiotherapy
  • External beam radiotherapy (EBRT)
    • Given in fractions e.g. delivered over 7 weeks
    • 3 dimensional conformal and intensity modulated techniques allow increased dose to be delivered to the prostate whilst minimizing dose to rectum and other structures
  • Brachytherapy
    • Seed brachytherapy involves permanently implanting radioactive seeds (iodine or palladium) into the prostate
    • High dose rate brachytherapy involved temporary insertion of a high dose radioactive source to give a boost of treatment to the prostate. It is usually combined with EBRT for high risk locally advanced disease

Complications include:

  • Bladder and bowel irritation e.g. proctitis
  • Impotence
  • Disease recurrence

*Cure rate rates may be less compared to surgery though no trial has compared this properly

  1. Androgen suppression
  • Prostate cancer is a testosterone dependent tumour
  • Androgens may be suppressed by:
    • Surgical castration
    • GnRH agonist e.g. Goserelin (Zoladex) and Leuprorelin (Lucrin)
      • Note there will be an initial increase in serum testosterone following administration of an LHRH agonist. Therefore an anti-androgen must be co-administered initially to cover this.
    • Anti-androgens e.g. cyproterone acetate, biclutamide
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7
Q

What % of macroscopic and microscopic haematuria end up being urothelial cancer?

A
  • Approximately 20% of macroscopic haematuria end up being bladder cancer
  • If there is microcytic haematuria (can’t see) - wait for 6 weeks and re-test, treat UTI etc. then refer to urologist (only 2% of these are cancer)
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8
Q

what is the most common histological bladder cancer

A
  • More than 90% are transitional cell carcinoma
  • A few are squamous cell carcinoma and adenocarcinoma
  • Male > Female (2.5:1)
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9
Q

Risk factors for bladder cancer

A
  • Age
  • Male sex
  • Smoking (500x)
  • Family history
  • Workers in certain industries exposed to carcinogens such as beta-naphthylamine, benzidine a rubber, textile/ dye industry, printing and metal
  • Drugs - such as cyclophosphamide
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10
Q

Investigations for potential bladder cancer (Haematuria)

A

Gold standard investigations:

  • Cystoscopy +/- biopsy for histology
  • Urine cytology – very specific but has low sensitivity (therefore, negative result does not mean cancer is not present)
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11
Q

Symptoms of bladder cancer

A
  • Painless gross haematuria through micturition (most common)
  • Irritative voiding symptoms (dysuria, urinary frequency, urgency)
  • Rarely bladder outlet obstruction
  • Ssuprapubic/ rectal/ perianal pain
  • Rarely palpable suprapubic mass (advanced)
  • Features of metastasis
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12
Q

Treatment of bladder cancer (carcinoma in situ, stage t1 and muscle invasion)

A

Carcinoma in-situ

  • Diagnosis by biopsy/ trans-urethral resection
  • Treatment with intravesicular immunotherapy – BCG (Bacillus Calmette-Guerin) with subsequent maintenance
  • Cystectomy if fails to respond to BCG

*Urothelial CIS represents a high grade risk form of urothelial cancer (unlike in-situ carcinoma in other organ sites. Though not showing invasion, it is at high risk of progression and should be aggressively managed

what is intravesicular BCG?

  • Live attenuated bacillus calmette-guerin
  • The BCG is instilled into the bladder via a catheter and then drained away weekly for 6 weeks and then monthly for one year
  • This is a form of immunotherapy and has been shown to decrease recurrence and progression of CIS and other high risk bladder cancer

At & T1 bladder cancer

  • TURBT (Transurethral resection of bladder tumour)
  • Intravesicular cytotoxics – using drugs such as mitomycin
  • Intravesicular immunotherapy – BCG

Muscle-invasive Bladder cancer

  • Radical cystectomy
  • Radiotherapy
  • Combined treatments – chemotherapy followed by radical cystectomy. Radiotherapy followed by chemotherapy

Importance of multi-modal therapy à Chemo + surgery

Cystectomy

  • Is a major surgery
  • Requires thorough cardiovascular and respiratory system evaluation, bowel prep, blood cross-matched and stoma education pre-operatively
  • An ileal segment is isolated on its mesentery and and end-to-end anastomosis is then performed to restore bowel continuity
  • Both ureters are anastomosed to portion of ileum resected to form stoma

Metastatic Disease

  • Systematic chemotherapy
  • Palliative radiotherapy – to relieve symptoms and improve quality of life
  • Palliative surgery – radical cystectomy and urinary diversion
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13
Q

Causes of Urinary tract obstruction

A

Renal

  • Nephrolithiasis
  • Sloughed off renal papilla (papillary necrosis in diabetes, sickle cell, pyelonephritis)
  • Urothelial carcinoma

Ureters

  • Intraluminal
    • Nephrolithiasis
    • Blood clot
  • Intramural
    • Ureteral stricture
    • Accidental surgical ligation
    • Urethral carcinoma
  • Extraluminal
    • Pregnancy
    • Neoplasm of cervix, ovaries, colon
    • Aortic aneurysm
    • Iliac artery aneurysm
    • Tubo-ovarian masses: endometriosis, prolapse, haematoma
    • Gastrointestinal mass: Crohn’s disease, diverticulitis
    • Retroperitoneal fibrosis (Ormond disease)

Bladder

  • Urothelial carcinoma
  • Neurogenic bladder
  • Flaccid neurogenic bladder (LMN): detrosuor areflexia 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 sympatheticcontrol 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.

Urethra

  • Benign Prostatic Hyperplasia
  • Prostatic Cancer
  • Stricture
  • Posterior urethral valves (congenital = children)

Mechanical

Kinked or plugged indwelling catheter

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14
Q

Clinical features of urinary obstruction

A

Acute

Upper UTO

  • flank pain, haematuria
  • nausea and vomiting

Lower UTO

  • urinary retention
  • suprapubic pain
  • palpable bladder

Chronic

Upper UTO

  • usually asymptomatic
  • hypertension
  • renal failure

Lower UTO

  • LUTS
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15
Q

Investigations for suspected Urinary tract obstruction

A

Lab tests

  1. Urinalysis
  • Proteinuria ?
  • Haematuria – may indicate stone or tumour
  • Crystals – may provide information about content of stone
  • bacteriuria, pyuria
  1. UEC
  • Elevated blood urea nitrogen
  • Bilateral UTO in or UTO in solitary kidney - Elevated serum creatinine
  1. Serum electrolytes
    * Hyperkalaemia is dangerous complication of renal failure
  2. FBC
  • Leukocytosis in UTI
  • Anaemia in chronic UTO

Imaging

  1. U/S
  2. CT- KUB
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16
Q

What are the different types of renal stones and which is most common

A
  1. Calcium oxylate (40%)
    Hypercalciuria, decreased pH, radiopaque
  2. Calcium phosphate (35%)
    Hyperparathyroidism, Raised pH
  3. Uric acid stones (10%)
    High uric acid, gout, decreased pH
  4. Struvite stones (Staghorn)
    UTI with urease-producing bacteria such as Proteus mrabillis, Klebsiella, raised pH
  5. Cystine
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17
Q

Clinical features of urolithiasis

A

Stones usually form in the collecting ducts of the kidneys but may be deposited along the entire urogenital tract from the renal pelvis to the urethra. Their localization and size determine the specific symptoms. Small kidney stones may also be asymptomatic.

  • Severe unilateral and colicky flank pain (renal colic)
    • Radiated anteriorly to the lower abdomen, groin labia, testicles, or perineum
    • Paroxysmal or progressively worsening
    • The area around the kidneys may be tender on percussion
  • Haematuria
  • Nausea, vomiting, reduced bowel sounds
  • Dysuria, frequency, urgency
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18
Q

Investigations for urolithiasis

A
  1. Urine dipstick (microscopic haematuria is present in > 90%) and MSU (Urinalysis)
  • Gross or microscopic haematuria
  • Pyuria, positive leukocyte esterase, positive nitrites, or bacteriuria suggest UTI
  • Urine pH
    • >7 suggests urea-splitting organism and struvite stones
    • <5 indicates uric acid stones
  • Urine microscopy – may detect crystals
  • Obtain a urine culture if signs of Uti
  1. Blood tests:
  • FBC– leucocytosis concomitant UTI
  • UEC – creatinine raised suggests acute kidney injury
  • Calcium
  • Phosphate
  • Uric acid
  • PTH, albumin
  1. Radiological tests:
  • CT-KUB – gold standard
  • IVU (intravenous Urethrogram)
  • RCPG (Retrograde Pyelogram)
  • USS renal tracts
  • X-ray à radiopaque (calcium-containin stones), radiolucent (uric acid stones)

Differentials need to be rules out – leaking abdominal aortic aneurysm, perforated peptic ulcer, peritonism. If haematuria is absent, question your diagnosis.

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19
Q

Prevention of renal stones

A
  • Sufficient fluid intake *>2.5L per day)
  • For calcium stones
    • Reduced consumption of salt and animal protein
    • Reduced consumption of oxylate-rich foods and supplemental vitamin C
    • Thiazide diuretics for recurrent calcium-containing stones with idiopathic hypercalciuria
    • for uric acid stones à allopurinol
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20
Q

treatment of urolithiasis

A

Ask yourself is this case complicated by:

  • High grade or infected hydronephrosis
  • Urosepsis
  • Acute kidney injury
  • Intractable pain and Vomiting

*Infected obstruction is a medical emergency

Haemodynamically stable patients without complicated stone < 7mm à trial of observation with symptomatic treatment to enable spontaneous passage

Urological intervention required for stones:

  • >7mm
  • complications above
  • failure to pass stone spontaneously in 4-6 weeks

Medical therapy

  1. Hydration
  2. Analgesia (NSAIDs, panadeine forte, indomethacin)
  3. Urology outpatient follow up
  4. Need to give dietary advice:
    • Increase fluid intake
    • Reduce intake of animal protein (meat, fish, poultry)
    • Avoid excessive high oxalate containing foods/ drinks e.g. tea, chocolate, spinach, rhubarb, okra, eggplant
  5. Medical expulsive therapy: alpha-blockers (tamsulosin) or calcium-channel blockers (nifedipine)
  6. Antibiotics if UTI

*For uric acid stones - urine alkalinisation

Surgical intervention

  1. Extracoroporeal shockwave lithotripsy
  2. Uteroscopy/ lasertripsy
  3. Percutaneous nephrolithotomy
  4. Laproascopic removal
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21
Q

Risk factors for developing testicular cancer

A
  • Cryptorchidism (Undescended testes)
  • Previous history of testicular cancer
  • Family history
  • Atrophy e.g. mumps, orchitis, trauma
  • Genetic syndromes (esp. klinefelter’s disease, down syndrome à Germ cell tumours
  • Subfertiliy
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22
Q

classification of testicular neoplasms

A

Primary (usual) and secondary (rare)

Germ cell tumours (95%)

  1. Seminoma (50% of cases)
    * Good radiosensitivity, slow growth, late metastasis, better prognosis than non-seminomas
  2. Non seminomatous germ cell tumours. Combination of:
  3. Yolk sac (5%)
    * Most common pre-pubertal testicular tumour
  4. Embryonal (20%)
    * Usually min mixed germ cell tumours, aggressive tumour
  5. Teratoma (20%)
    * Rare in adults, common in children
  6. Choriocarcinoma
    * Most aggressive

Non germ cell tumours (Non-GCTs)

  1. Lymphoma (Common in > 50 years) usually non-hodgkin
  2. Leydig cell tumours (1-3%) – these produce testosterone – may produce androgenic symptoms
  3. Sertoli cell tumours (<1%) – these cells nourish the sperm
  4. Other
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23
Q

clinical features of testicular cancer

A
  • Usually presents as painless lump
  • Negative transillumination test
  • Dull lower abdominal or scrotal discomfort more common than acute scrotal pain
  • Patient frequently recalls a non-significant testicular trauma or event
  • Occasionally present with acute testicular pain, hydrocele, or metastatic disease
  • In metastatic disease – cough, SOB, chest pain
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24
Q

Investigations for testicular neoplasm

A

Produce characteristic serum tumour markers which should be monitored before, during and after treatment

  • Tumour markers are raised in:
    • 50% of tumours
    • up to 90% of advanced tumours
  1. Alpha feto Protein
    • Half-life: 5-7 days
    • Produced by foetal gut, liver, yolk sak
    • Elevated in liver, pancreatic, stomach and lung tumours. Also raised in normal pregnancy and benign liver disease
  2. B-hCG
    • Half life: 24-36 hours
    • It implies syncytiotrophoblastic component (choriocarcinoma)
    • Produced by placental tissue
    • Produced by many subtypes especially choriocarcinoma
  3. LDH
    • Non-specific tumour marker, measures burden of metastatic disease

Imaging

  1. U/S
  2. CT chest/ abdomen/ pelvis
    • Used to stage the disease

Confirmation

  • Histopathological confirmation following radical inguinal orchiectomy
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25
Q

Staging of testicular cancer includes:

A
  • TNM staging
  • Also has an S classification which includes present of tumour markers - LDH, hCG, AFP
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26
Q

treatment of testicular cancer

A
  • Removal of the affected testicle is urgent
    • Ca testis = one of the fastest doubling times of all malignancies
    • Patient should be referred to urologist without delay
  • Urologist removes testicle + cord through inguinal canal, rather than the scrotum
    • Enables early control of venous drainage prior to manipulating
    • Avoids seeding the scrotal tissues with cancer cells
    • Removes initial lymphatic drainage pathway of testicle (via cord)
  • Most patients have chemotherapy or radiotherapy after orchidectomy
    • Depends on stage – surveillance may be offered for stage I
    • Depends on tumour subtype
      • Seminoma are very radiosensitive and chemosensitive
      • Non-seminomas are very chemosensitive

Prior to treatment

  • Patients should be offered sperm banking
  • Serum markers should be sent
  • Patients disease should be staged (CT chest/ abdomen and pelvis)
  • Patient may be offered a prosthesis (artificial testicle) by their urologist

After treatment

  • Patient require prolonged follow up (10y+)
  • Recurrence can occur many years down the track
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27
Q

Causes of Urinary Retention

A

Mechanical obstruction

  • Enlarged prostate
  • Benign Prostatic Hypertrophy
  • Prostate cancer
  • Acute prostatitis
  • Urethral Narrowing
  • Urethral stricture
  • Urethral carcinoma
  • Posterior urethral valves
  • Urethritis
  • Meatal stenosis (rare)
  • Bladder neck obstruction
  • Bladder calculi
  • Urothelial cancer
  • Urinary bladder tamponade
  • Phimosis and paraphimosis
  • Blocked catheter

Functional

  • Detrusor underactivity and/or sphincter overactivity
  • Neurological Causes
  • CNS
  • Stroke
  • Spinal cord compression
  • Multiple Sclerosis, Parkinson’s Disease
  • Peripheral nervous System
  • Damage to pelvic splanchnic nerves (bladder denervation) à causes ¯ bladder sensation and detrusor contractility à infrequent, incomplete urination à overflow incontinence
  • Diabetic autonomic neuropathy
  • Trauma (pelvic fracture, surgery/ radiation of pelvis)
  • Drug-induced urinary retention
  • Due to detrusor underactivity: anticholinergics, tricyclic antidepressants, antipsychotics, calcium channel clockers, antiparkinson agents
  • Due to increased urethral sphincter tone: sympathomimetic agents, nonselective beta blockers, opioids
  • Detrusor-sphincter dyssynergia
  • Urethral/ bladder trauma (urethral transection)
  • Post-op urinary retention
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28
Q

Clinical features of urinary retention

A

Acute

  • More common in men >70
  • Sudden, painful inability to void despite having a full bladder
  • Suprapubic pain/ discomfort; palpable bladder
  • Patient is restless and distressed

Chronic

  • Females > males
  • Chronic, painless incomplete voiding of the bladder
  • Palpable bladder may be present
  • May present with overflow incontinence or nocturnal enuresis
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29
Q

Investigations for urinary retention

A

Lab studies

  1. Urinalysis and culture – evaluate for UTI, haematuria, glycosuria, and crystals
  2. U&E – BUN (Blood urea nitrogen, Creatinine levels, electrolytes): evaluate for renal failure (obstructive nephropathy)
  3. PSA – serum prostate specific antigen
  4. BSL - glucose control in known diabetics or if diabetic neuropathy is suspected

Imaging

  1. U/S of kidney, ureter and bladder (indicated in all patients with urinary retention)
  • AUR – bladder distented with > 400mL or urine
  • CUR – post void residue > 300mL; bladder wall thickening
  • In both evaluate for hydroureteonephrosis; diagnose bladder calculi or BPH

Further investigations

  1. Transrectal U/S – prostate cancer
  2. Cystoscopy – suspected bladder cancer (gross haematuria)
  3. Retrograde urethrogram or voiding cystourethrogram – urethral trauma, stricture, tumours
  4. Pelvic U/S
  5. MRI brain or spinal cord
  6. Urodynamic studies
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30
Q

What is renal cell carcinoma and what are its risk factors

A

RCC arises from renal tubular epithelium, is the most common cause of renal malignancy in adults (85%)

Risk factors

  • Smoking
  • Family history
  • Certain pre-existing conditions
  • Renal pelvic stones
  • Obesity
  • Hypertension
  • Acquired cystic kidney disease as a result of ESRD
  • Immunodeficiency
  • Sickle cell disease
  • Chronic hepatitis C infection
  • Occupational exposures
  • Occupational exposure to cadmium, asbestos and/ or petroleum
  • Chemotherapeutic agents (cisplatin) during childhood
  • Chronic analgesic use (aspirin, acetaminophen)
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31
Q

Features of renal cell carcinoma

A

Classic triad of:

  • Haematuria
  • Flank pain
  • Abdominal mass

Also:

  • Anaemia (common), pallor, lethargy
  • Constitutional symptoms: weight loss, fatigue, night sweats

RCC asymptomatic in early stages. Patients become symptomatic when the tumour has reached a large size (usually > 10cm) and/ or if metastases are present

Paraneoplastic syndromes:

  • Hypertension
  • Hypercalcaemia
  • Polycythemia, leukemoid reaction
  • Secondary hypercortisolism
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32
Q

Evaluating renal cell carcinoma investigations

A

Imaging

  1. Abdominal CT scan with contrast
  2. Renal U/S

Evaluation of metastatic disease

  1. CT/ MRI of the thorax
  2. Bone scan

Lab tests

  1. Urinalysis – haematuria
  2. Hb levels and FBC
  3. Hypercalcaemia
  4. Raised AST, ALT and/ or ALP
  5. BUN/ creatinine
  6. Percutaneous renal biopsy is generally not recommended
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33
Q

Treatment of RCC

A

Surgical resection of the tumour

  • Stage I: cryoablation, thermal ablation, partial nephrectomy, or simple nephrectomy
  • Stage II-IV: radical nephrectomy

RCC is resistant to chemotherapy and radiotherapy

New drugs

  • Interferon-alpha
  • Tyrosine kinase inhibitors e.g. sorafenib, sunitinib
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34
Q

What does BPH stand for and describe the epidemiology of it

A

Benign prostatic hyperplasia

  • Refers to increased prostate size due to increased cell number (NOT bigger cells)
  • This hyperplasia of prostatic stromal and epithelial cells results in nodular growth in the prostatic urethra

Epidmeiology

  • 50% of 50-60yo
  • 80% of 80yo
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35
Q

Symptoms of BPH

A

Continued enlargement can block the urethra, which can cause lower urinary tract symptoms (LUTS)

  • Frequency
  • Incomplete emptying
  • Hesitancy
  • Intermittency
  • Urgency
  • Weak stream
  • Straining
  • Nocturia

BPH = Bladder outflow obstruction + lower urinary tract symptoms + benign prostatic enlargement

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36
Q

complications of BPH

A
  • Urinary retention
  • UTI
  • Urosepsis
  • Urinary bladder stone
  • Obstructive uropathy and renal failure
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37
Q

Investigations for BPH, and what is the IPSS and its use

A
  • History of LUTS - IPSS is commonly used symptom score
  • Rectal examination - smooth enlarged prostate
  • PSA - very low PSA makes BPH unlikely. Prostate cancer may co-exist.
    Note: PSA elevated is not diagnostic of BPH or prostate cancer. It is reported symptoms, imaging, urodynamics and sometimes prostate biopsy that leads to diagnosis of BPH
  • Trans-rectal U/S and biopsy - a prostate biopsy is performed to detect prostate cancer in patients with an abnormal DRE and/ or increased PSA. A negative biopsy helps confirm a diagnosis of BPH

PSA

  • Is a serine protease produced by the prostate involved in the liquefaction of sperm
  • Is prostate specific but not cancer specific
  • Serum PSA increases with age, increasing size of prostate and in prostate cancer
  • Serum PSA can be elevated in urinary infections or after surgical instrumentation

IPSS – International Prostate Symptom Score

  • Based on 7 questions and gives a measure of symptoms and how badly these symptoms are affecting life
  • It also allows urologists to assess patients response to therapy and disease progression
  • Score of 0-7 = mildly symptomatic, score 8-19 = moderate, 20-35 = severe
  • IPSS does not establish a diagnosis of prostate cancer or BPH
  • Questions:
    • Incomplete emptying
    • Frequency
    • Intermittency
    • Urgency
    • Weak stream
    • Straining
    • Nocturia
38
Q

Treatment for BPH

A

Medical Treatment of BPH

  1. Alpha Blockers (Alpha1-adrenergic antagonist)
  • Prazosin, tamsulosin 0.4mg OD
  • Tamsulosin is more uro-selective
  • Relaxes smooth muscle in the prostate gland and bladder neck improving urinary flow
  • Common side effect is Postural Hypotension
  1. 5 alpha-reductase inhibitors
  • Finasteride (Proscar) 5mg OD, Dutasteride
  • Inhibits 5a-reductase, an enzyme which is responsible for the conversion of testosterone to dihydrotestosterone (DHT) in prostate
  • DHT is known to be responsible for the enlargement of the prostate gland
  • It is also used for the treatment of male pattern baldness
  • Side effects (approx. 5 %): erectile dysfunction, loss of libido, breast tenderness
  • 2 drugs are available – finasteride and dutasteride which reduce DHT production by inhibiting one or both of the isoenzymes of 5 alpha reductase respectively
  1. Anticholinergics
  • Treat symptoms of over-active bladder (Storage symptoms)
  • Common side effects include dry mouth and constipation. Rarely blurred vision and confusion
  • Contra-indicated in glaucoma, avoid in the elderly
  • May precipitate urinary retention (avoid in bladder outflow obstruction)

*A combination of alpha-blocker and a 5-alpha-reductase inhibitor is sometimes required

Surgical treatment of BPH

Indications for surgery

  • Severe symptoms
  • Failed medical treatment
  • Complications of bladder outflow obstruction: urinary retention, bladder stones, UTI, upper tract obstruction/ renal impairment

Types of surgery

There are several types of surgery available

  1. Transurethral resection of the prostate (TURP)
  2. Laser ablation/ resection
  3. Open prostatectomy

TURP

  • Patient has mainly storage symptoms not voiding symptoms
  • Performed under spinal or GA
  • Involves inserting a cystoscope and an electrical loop that cuts and diathermies bleeding vessels in the prostate gland
  • Irrigation fluid is also passed through the cystoscope. Commonly used irrigation fluid is glycine
  • Prostate chips that have been removed will be sent off for histopathology
  • Patients are expected to stay in hospital for approximately 1-2 days post-op. recovery for most patients is about 2 weeks
  • IDC is inserted at end of operation and remains in-situ for the first 24-hour post-op

Risks

  • Bleeding, infection, retrograde ejaculation, erectile problems, urinary incontinence, bladder neck stricture
  • TURP syndrome. This is a dilutional hyponatraemia after absorption of hypotonic irrigation solution used during the procedure.

When to think hard/ investigate further before offering TURP?

  • Over 80s and under 50s
  • Possible neurogenic cause for symptoms (CVA, diabetic)
  • Previous TURP
39
Q

What is testicular torsion and what is the deformity that predisposes to it

A

Testicular torsion is the sudden twisting of the spermatic cord within the scrotum. It most commonly affects children and young men. Because of the risk of ischaemia and possible infarction of the testicle, it is considered a urological emergency.

Bell-Clapper Deformity

High fusion of tunica vaginalis means testicle lies loose in bell-clapper configuration

  • Enables testicle to twist around on its blood supply
  • Bell clapper testicles tend to be high riding with a horizontal lie
40
Q

Clinical features of testicular torsion

A
  • Abrupt onset testicular pain and/ or pain in the lower abdomen
    • Typically swollen and tender testicle and/ or lower abdominal tenderness
  • Nausea and vomiting
  • Abnormal position of testicle
    • Abnormal transverse lie
    • Scrotal elevation
    • Possible undescended testes (predisposes to testicular torsion)
  • Absent cremasteric reflex
  • Prehn sign: negative
    • Positive if lifting the testicle relives pain (typical for epididymitis), negative if it doesn’t (typical for testicular torsion).

*Testicular torsion should always be suspected in a male patient with severe, sudden-onset testicular pain

41
Q

What investigations would you do for testicular torsion (kind of a trick question)

A

If there is clinical suspicion of torsion, patient should be referred to Urology without further investigation

Lab tests

  • Urine dipstick to exclude epididymitis
  • Inflammatory markers in case of epididymitis, FBC, UEC

U/S

  • Indications: ambiguous clinical findings, low suspicion of testicular torsion
  • Doppler U/S reduced perfusion in the affected testicle

*Surgical intervention is recommended for suspected testicular torsion, regardless of radiological findings

42
Q

Treatment of testicular torsion

A

Emergency exploration of BOTH testis, torted side first

  • Testicle is immediately de-torted
  • Viability assessed after warming in saline packs
  • Testis viable after de-torsion – 3 point fixation (orchidopexy) to pin testicle and tunica vaginalis onto dartos muscle of the scrotum
    • Contralateral side also explored and fixed because this condition is BILATERAL
    • Failure to treat the other side will result in future torting of the untreated testicle
  • Testis non-viable after de-torsion – orchidectomy and then fixation of contralateral side
43
Q

What are some complications of undescended testes

A
  • infertility
  • testicular cancer
  • testicular torsion
  • inguinal hernia
44
Q

treatment for undescended testis

A

Surgery is recommended between 6-18 months of age

  • Orchidopexy: exposure and fastening of the testicles to the scrotum
  • Non-palpable testes: potentially therapeutic open or laparoscopic orchidopexy
45
Q

What is vesicoureteral reflux

A

Vesicoureteral reflux is the retrograde flow of urine from the bladder into the ureter. Primary VUR is the most common type and is due to a congenital defect of the terminal portion of the ureter.

Epidemiology

  • Incidence: 1% of newborns
  • Prevalence of VUR
    • Among children with UTIs: 30-45%
    • Among neonates with prenatal hydronephrosis: 15%
  • Age; children < 2
  • Females > Males (2:1)
  • More common in white children
46
Q

Causes of vesicoureteral reflux

A

Primary VUR (Most common): Short intramural ureter - vesicoureteric junction (VUJ) fails to close completely during bladder contraction - VUR

Secondary VUR

  • Bladder outlet obstruction (anatomic/ functional): high pressure within the bladder - reflux of urine through the VUR
    • Anatomical: Posterior urethral valves; urethral meatal stenosis
    • Functional: bladder and bowel dysfunction; neurogenic bladder
    • Cystitis
  • Congenital anomalites of the ureter
    • Ureteral duplication
    • Ectopic ureter
    • Ureterocele
47
Q

clinical features of vesicoureteral reflux

A
  • Suspected in the prenatal period when hydronephrosis is detected on routine antenatal U/S
  • Postnatal presentation
    • Recurrent febrile UTIs
      • Neonates: irritability, fever, listlessness
      • Older children: urinary urgency, frequency, incontinence, dysuria associated with fever
    • Reflux nephropathy (A type of interstitial nephritis): renovascular hypertension, kidney failure, uraemia
    • Flank or abdominal pain before or during voiding

*VUR is generally asymptomatic until it causes a UTI

48
Q

Investigations for vesicoureteral reflux

A

Lab studies

  • Urinalysis and urine culture: indicated in all children with hydronephrosis to rule out infection
  • UEC
    • Uremia may be present in bilateral VUR because of renal parenchymal scarring (secondary to reflux of infected urine) or an associated congenital renal hypoplasia.

Imaging

  1. U/S
    • indicated in children with febrile UTI
    • detection of hydronephrosis and dilater ureter
  2. Contrast voiding cystourethrogram
    • Indicated for children with > 2 episodes of febrile UTI, or UTI with hypertension, significant fever
    • Contrast instilled through urethral catheter. Retrograde reflux of contrast into ureters during micturition is diagnostic of VUR
  3. Urodynamic testing to evaluate secondary VUR
    * A group of tests to assess function of the urinary tract and to identify sites of obstruction. Includes cystometry (evaluates bladder function during filling, storage, and voiding), uroflowmetry (evaluates rate of urine flow), and urethral tests (evaluate intrinsic sphincter function). Indicated in the diagnostic workup of lower urinary tract dysfunction and for the planning of surgical treatment.
49
Q

Treatment for VUR

A

Conservative

Indicated for VUR grades I-III in children < 5 years of age

  1. Long term prophylactic antibiotics
    • Children > 3mo à nitrofurantoin
    • Infants à amoxicillin
  2. Behavior modification e.g. timed voiding, prevention of constipation
  3. Surveillance: urinalysis, renal imaging

Surgical

Indicated for VUR >= grade IV. Bilateral grade III, especially children > 6yo. OR worsening renal function/ breakthrough UTIs despite prophylactic antibiotics

  1. Subureteric transurethral injection
  2. Ureteral reimplantation
50
Q

What is prostatitis and its causes

A

Inflammation of the prostate gland that may be infectious (acute and chronic bacterial prostatitis) or non-infectious (Chronic pelvic pain syndrome)

Bacterial prostatitis

Gram-negative bacteria, particularly E.coli and other Enterobacteriaceae

Risk factors:

  • other genitourinary tract infections e.g. urethritis, cystitis, epididymitis
  • genitourinary tract interventions e.g. indwelling catheter, transurethral surgery

Chronic pelvic pain syndrome

No detectable causative organism. The exact aetiology unknown

51
Q

clinical features of prostatitis

A

Acute bacterial prostatitis

  • fevers, chills
  • acute dysuria, frequency, urgency, cloudy urine
  • severe genitourinary pain
  • prostate is tender and swollen

Chronic bacterial prostatitis

  • chronic bladder irritation - dysuria, frequency, urgency
  • mild genitourinary pain

Chronic pelvic pain syndrome

  • moderate genitourinary pain
52
Q

investigations for prostatitis

A

Lab tests

Acute bacterial prostatitis

  1. Urinalysis using MSU
    • Raised WCC, urine culture, urine gram stain (E.coli most commonly seen)
  2. Blood tests
    • Raised inflammatory markers
    • Raised PSA
  3. Blood cultures is sepsis suspected

Chronic bacterial prostatitis

Stamey test – sequential urine cultures (not really used anymore)

  • Voided bladder 1: initial 5-10mL or urine specimen 

  • Voided bladder 2: clean-catch midstream urine specimen 

  • Expressed prostatic secretions; secretions expressed from prostate by digital massage after 
midstream urine specimen 

  • Voided bladder 3: first 5-10 mL of urine stream immediately after prostatic message 


Further tools

  • Urethral swab and culture
  • U/S to assess residual urine
  • Cystoscopy
53
Q

management of bacterial prostatitis

A
  1. Fluroquinolones (ciprofloxacin)
  2. Suprapubic catheterization in cases of acute urinary retention and persistent fever
54
Q

What is hydrocoele and its clinical features

A

Painless accumulation of fluid in a sac around one or both testicles which derived from the tunica vaginalis, a tissue covering the testes.

Features

  • Fluctuant, painless swelling of affected scrotum
    • May be present since infancy or childhood
    • May or may not be reducible
  • Palpation above the swelling is possible (not the case in hernia): a normal spermatic cord and inguinal ring are present
  • Positive transillumination
55
Q

Investigations for hydrocoele

A

Usually clinical

  1. Inguinoscrotal U/S is highly sensitive, specific, reliable and reproducible. It should be performed to confirm diagnosis and exclude malignancy

When diagnosing hydrocele it is important to exclude testicular ancer, infection/ abscess, trauma/ rupture of testis

56
Q

Treatment of hydrocoele

A

Usually resolves spontaneously within 6 months of birth

Indications for surgery:

  • If spontaneous resolution does not occur in children by 1 year of age
  • Excessive discomfort and/ or if scrotal skin integrity is compromised
  • An underlying pathology is suspected
  • Testicle not palpable
  • If infertility is a concern

Procedures

  • Aspiration rarely indicated as risks infection and collection rapidly recurs
  • Surgery e.g. hydrocoelectomy with plication and/ or eversion of tunica vaginalis are used most commonly
    • Recurrence rate is low
    • Post-op haematoma is a common complication
57
Q

What is varicocoele and its clinical features (what side most commonly effected)

A

Abnormal enlargement and tortuosity of the pampinoform plexus in the scrotum due to proximal obstruction the spermatic vein.

Features

  • May be painless enlargement
  • Dull, aching pain of the hemiscrotum (typically left-sided)
  • Heaviness of the affected scrotum
  • Soft bands/ strands are palpable in the upper pole of the affected scrotum (feels like a bag of worms)
  • Symptoms worsen when standing or when performing a Valsalva maneuver
  • Negative transillumination
58
Q

Investigations for varicocoele and causes

A

Investigations

  1. Inguinoscrotal U/S is highly sensitive, specific, reliable and reproducible. It should be performed to confirm diagnosis and exclude malignancy

When diagnosing varicocoele it is important to measure size of testis and check the kidneys for tumour (occassionally cause varicocoele)

Causes

  • Primary
    • Mainly left‑sided: the left spermatic vein is a long vein with high pressure because of its position between the aorta and superior mesenteric artery. Dilation of the spermatic vein, which is positioned perpendicular to the renal vein → obstruction of the spermatic vein → poor outflow of blood and stasis → varicocele
  • Secondary
59
Q

treatment for varicocoele

A

Invasive treatment indications:

  • Adolescents with testicular atrophy or delayed growth of the affected testivle
  • Adult men with evidence of infertility (confirmed with an abnormal sperm analysis)

Procedure: Laparoscopic varicocelectomy or percutensous embolization

Conservative management (indicated in older patients)

  1. NSAIDs
  2. Scrotal Supports

Young men without testicular atrophy or evidence of infertility should recive follow ups (regular assessment of testicle size and/ or semen analysis every 1-2 years)

60
Q

Urinary tract infections comprise of; cystitis, pyelonephritis and aymptomatic bacteriuria. What are these?

A
  1. Cystitis – infection of the bladder (lower urinary tract infection)
  2. Pyelonephritis – infection of the parenchyma and collecting system of the kidney (upper urinary tract infection)
  3. Asymptomatic bacteriuria – significant bacteriuria present in the urine with no symptoms (usually seen in children, pregnant and elderly)
61
Q

Risk factors for UTI

A
  • Female - shorter urethra
  • Sexually active
  • Menopause, pregnancy
  • Renal calculi
  • Vesicoureteral reflux
  • Immunocomprimise
  • Age - small kids, pregnant, older age
  • Residual bladder in urine
    • neurogenic bladder
    • urethral stricture
    • BPH
  • Instrumentation of the urinary tract
    • IDC
    • Cystoscopy
    • Urethral dilation
62
Q

Common UTI Pathogens

A

Community acquired

  • Escherichia coli
  • Staphylococcua saprophyticus
  • Less commonly Proteus Enterobacter

Hospital acquired

  • E.coli
  • Enterobacteriaceae
  • Pseudomonas aeruginosa
  • Enterococcus faecalis
63
Q

Symptoms of UTI

A

Cystitis

  • Dysuria
  • Frequency
  • Urgency
  • Urine is turbid, may smell offensive, may be bloody

Pyelonephritis

  • Flank or back pain
  • fevers, chills, rigors
  • headache, nausea, vomiting
  • dysuria, frequency, urgency
64
Q

investigations for UTI

A

Urine can be easily contaminated by the same bugs that cause UTIs.

  1. Urine dipstick
    * Nitrate and leukocyte esterase positive
  2. Urine microscopy
    * White Cells
  • Values above 10x10^6 indicate inflammation of urinary tract
  • If urine left standing, leucocytes breakdown, so prompt processesing
  • Elevated WCC in urine = pyuria –> cloudy beer appearance
  • Red cells
  • Indicate bleeding in urinary tract (calculi, tumours, inflammation, infection); or from being extruded through damage glomeruli (glomerulonephritis)
  • Extruded red cells from glomeruli have bizarre morphologies
  • Red cells with normal morphology seen in UTI
  • Note menstruations is common source of red cells
  • Squamous epithelial cells
  • Originate outside urinary tract, presence indicates contamination
    1. Urine culture
  • Quantitative culture; UTI if:
  • Adult female: > 10^2/mL (>10^5/L)
  • Adult males: > 10^3/mL
65
Q

Treatment of Cystitis and Pyelonephritis

A

Cystitis

  • Amoxicillin
  • Augmentin
  • Cephalexin 500mg orally, 12 hourly for 5 days
  • Nitrofurantoin 100mg orally, 6-hourly for 5 days
  • Trimethoprim 300mg orally, daily for 3 days
  • Norfloxacin

Pyelonephritis

Non-severe –> Amoxicillin + Clavulanate 875+125mg orally, 12 hourly for 14 days

Severe –> Gentamicin IV + amoxicillin

66
Q

Definition of CKD

A

An estimated or measured GFR < 60mL/min/1.73m^2 that is present for > 3 months with or without evidence of kidney damage

Evidence of kidney damage with or without decreased GFR that is present for > 3 months as evidenced by the following:

  • Albuminuria
  • Haematuria after exclusion of urological causes
  • Structural abnormalities (e.g. on kidney imaging tests)
  • Pathological abnormalities (e.g. renal biopsy)
67
Q

Risk factors for CKD

A
  • 60 years or older
  • Diabetes
  • Family history
  • Established CVD
  • Hypertension
  • Obese
  • Smoker
  • Indigenous
  • History of AKI
68
Q

Most common causes of CKD

A
  • Diabetic nephropathy (1/3rd)
  • Glomerulonephritis
  • Hypertensive vascular disease
  • Polycystic kidney disease
  • Reflux nephropathy
  • Other – vasculitides etc.
69
Q

Clinical features of CKD and its complications (Think of complications through the NEPHRON acronym used to treat CKD)

A

Symptoms

  • Stages 1-3 often asymptomatic
  • Fatigue
  • Nausea
  • Loss of appetite
  • Haematuria
  • Oedema
  • Muscle weakness
  • Anaemia
  • SOB
  • Peripheral neuropathy
  • Oliguira

Complications

N – Nitrogen

  1. Uraemic Pericarditis, Pleuritis, Encephalopathy

E – Electrolytes

  1. Hyperkalaemia – Normal maintained unless aldosterone secretion (ACEIs, ARBs, B-blockers). Treat with insulin and risonium)
  2. Hyperphosphataemia – early in disease course. As GFR decresses phosphate is excreted.
  3. Hypocalcaemia – hyperphosphataemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D to calcitriol, calcitriol usually stimulates the absorption of Ca++ from the GI
  4. Hyperparathyroidism – secondary to hyperparathyridism in response the hypocalcaemia caused by CKD

P – pH

  1. Metabolic acidosis – H+ ions buffered into cells, RBCs, bones and albumin buffer

H – Hypertension

  1. HTN – Decreased GFR results in increased renin secretion and stimulation of the RAAS. Fluid retention and HTN which further worsens kidney disease.
  2. CVD risk factor

R – Red Blood Cells

  1. Anaemia – Normochromic Normocytic Anaemia. Decreased renal synthesis of EPO that stimulates BM cells to produce RBCs decreases bone and bone marrow quality-renal osteodystrophy. Anaemia of chronic disease.

O – Osteodystrophy and Oedema

  1. Renal osteodystrophy – high bone turnover lesions with increased PTH secretion (oseitis fibrosa). Given vitmain D. bisphosphonates – complications long term.
  2. Volume overload – kidneys responsible for excreting Na+ and water. As function declines there is Na+ and thus water retention and extracellular volume expansion leading to peripheral oedema and HTN. Clinical manifestations of volume overload occur in severe CRF < 15. Tubulointerstitial disease can cause fluid loss rather than overload.

N – Nephrotoxic drugs need to be stopped

  1. Pericarditis – due to uraemia
70
Q

Investigations for CKD

A
  1. Blood tests
  2. UEC
    1. Creatinine – increased
    2. eGFR
    3. Urea
    4. Electrolytes – hyperkalaemia, hyperphosphataemia, hypocalcaemia
    5. Bicarbonate, pH – metabolic acidosis
  3. Calcitriol (vitamin D) – decreased
  4. PTH – increased (Aiming to lower to 2-3 times upper normal, if not managed à adynamic bone desease)
  5. Coagulation testing – increased bleeding time
  6. Fasting lipids – patients at CVD risk **CVD is what kills most patients with CKD**
  7. FBC - Hb
  • Anaemia of chronic disease (Decreased MCV)
  • Function of kidney is to produce EPO
  1. Urinalysis – albuminuria, urine sediment abnormalities
  2. Ultrasound
  • Shrunken kidneys and fibrotic parenchyma, hydronephrosis
  • Polycystic kidney disease?
  • In diabetes – kidneys tend to be larger
  1. CT – masses + cyst
  2. Renal biopsy to confirm specific diagnosis of CKD – histological abnoramlaities (See Diabetic nephropathy for an example)
71
Q

Treatment of CKD

A

N - Nitrogen and sodium low diet

  • Sodium restriction in patients with oedema or hypertension
  • Monitor fluids and body weight to prevent oedema

E – Electrolyte monitoring

  • Treat hyperkalaemia – risonium (potassium binder)
    • ECG changes - peaked T waves, flatted P waves, long PR
  • Hyperphsphataemia – phosphate binding medications
  • PTH axis controlled

P – Ph monitoring and Proteinuria

  • Can reduce proteinuria by stating on ACE-I or ARB – big improvement in mortality

H – Hypertension Treatment

R – Red blood cells

  • synthetic EPO à Dabapoitein
  • Iron replacement, monitor serum ferritin

O – Osteodystrophy

  • Calcium supplementation + Vitamin D
  • PTH goes very high, try keep it down to no more than 3 times normal high limit

N – Nephrotoxic drugs stopped

  • NSAIDs, nicotine, acyclovir, vancomycin, cisplatin, contrast

Additiona…

Reduce CVD risk

  • Smoking cessation
  • Activity, diet
  • Statin, antihypertensive

Treat Underlying Cause

  • Manage Diabetes, monitor HbA1c (increase insulin)

If Significantly Fluid overloaded

  • Frusemide – 200mg BD IV
  • Monitor fluid levels and daily weights

Vaccination

  • For influenza (yearly) and pneumococcal (5 yearly)

Progression to Dialysis

  • Absolute Indications – pericarditis (pericardial rub), pleuritis, uraemic encephalopathy
  • Other indications – GFR < 15 and symptomatic
  • Types of dialysis
    • Peritoneal (continuous or nightly)
    • Haemodyalysis – usually a few days a week at hospital (4 hour sessions)

Transplant?

72
Q

What are the functions of the kidney

A
  • pH and volume regulation, Electrolyte balance
  • BP regulation
  • Endocrine function –> EPO
  • vitamin D synthesis
  • Control rate of RBC production
  • Remove metabolic waste
73
Q

Causes of acute renal failure (Pre-renal, renal, post-renal)

A

Pre-renal

  • Absolute decrease in circulating blood volume - dehydration, blood loss
  • Cardiac pump failure - MI, CCF
  • Effective decrease in blood volume - Sepsis, neurogenic, Vasodilatory drugs (NA, Adren)
  • Obstruction to circulation - Constrictive pericarditis, cardiac tamponade, PE
  • Locally reduced renal perfusion - Renal artery or vein occlusion

Renal

  • Acute tubular necrosis
  • glomerulonephritis
  • Interstitial nephitis

Post-renal

  • Ureter - stone, blood clot, tumour
  • Lower - BPH, urethral stricture
  • Blocked catheter
74
Q

Symptoms of acute renal failure

A
  • Symptoms of underlying illness causing AKI
  • Oliguria or anuria
  • Lethargy
  • Vomiting
  • Oedema
  • Weight loss/ anorexia
  • Sleep disturbances
  • Pruritis
75
Q

Investigations for AKI

A
  1. Blood tests
  • Creatinine - Acute increase in serum creatinine and decrease in urine output
  • FBC – anaemia or leukocytosis
  • VBG - Metabolic acidosis
  • U&E – Hyperkalemia (ECG), hypocalcaemia
  • BUN: Creatinine ratio
    • Raised - pre-renal, lowered - renal
  1. Urinalysis
  • Albuminuria
  • RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase
  1. Urine microscopy – reveals hyaline casts in pre-renal AKI
  2. Urine culture
  3. U/S – may reveal urinary tract obstruction
  4. Biopsy – in suspected rapidly progressive glomerulonephritis
  5. CXR if suspect pulmonary oedema from fluid retention
76
Q

Criteria for AKI

A

Any of the following

  • Rise in creatinine > 26umol/L in 48 hours
  • Rise in creatinine > 1.5 baseline
  • Urine output < 0.5mL/kg/hr for > 6 consecutive hours
  • Urine output < 400mL/24 hours
77
Q

Treatment for AKI

A
  1. Treat underlying cause
  2. General stuff
    • Review medications and cease nephrotoxic drugs
    • Monitor and correct electrolyte imbalances and acidosis e.g. hyperkalemia, pH
    • Volume overload - diuresis
    • Remove outflow obstructions e.g. catheterization. Insert a new one and monitor fluid balance
    • If necessary - dialysis

Pre-renal

  • Blood loss requiring crystalloid or colloid?
78
Q

Epididymo-orchitis pathogens

A

Common infectious causes in men < 35:

  • Neisseria gonorrhoea
  • Chlamydia trachomatis

Common infectious causes in men > 35:

  • E. coli
  • Other coliforms
  • Pseudomonas species
79
Q

Investigaitons for epididymo-orchitis and treatment

A
  1. Gram stain or urethral secretions à presence of gram –ve diplococci
  2. Urine dipstick test – positive leukocyte
  3. Urine microscopy
  4. Urine culture
  5. NAAT or urethral secretion or first void urine for chlamydia and gonorrhoea

Treatment

  • Gonorrhoea - Ceftriaxone 500mg IMI or IVI plus azithromycin
  • Chlamydia - Doxycycline 100mg for 7 days +/- ceftriaxone 300mg IMI for gonorrhoea
80
Q

Urinary incontinence causes

A

Neurological causes

  • Multiple sclerosis
  • Parkinson’s disease
  • Stroke
  • Dementia
  • Spinal injury

Genitourinary causes

  • Trauma to the pelvic floor
  • Intrinsic sphincter deficiency
  • Urethral hypermobility in women
  • Impaired detrusor contractility
  • Bladder outlet obstruction e.g. bladder cancer
  • Pelvic floor weakness
  • Urogenital fistula
  • Renal stones

DIAPPERS (reversible causes of incontinence)

D – Delirium

I – Infection

A – Atrophic Urethritis/ vaginitis

P – Pharmaceutical e.g. diuretics

P – Psychiatric causes (depression)

E – Excessive urinary output (hyperglycaemia, CHF)

R – Restricted mobility

S – Stool impaction

81
Q

types of urinary incontinence

A
  • Stress - increased abdominal pressure –> urination
    e. g. weak pelvic floor muscles
  • Urge incontinence - inflammatory or neurogenic conditions
  • Overflow incontinence - impaited detrusor contractibility, outlet obstruction
  • Functional incontinence
82
Q

investigations for urinary incontinence

A

Neurological, vaginal and rectal exam

Voiding diary to assess frequency and volume of micturition

review medications

Lab tests

  1. Urine MC&S – to exclude urinary tract infections
  2. Urea and electrolytes
  3. Creatinine and blood urea nitrogen (BUN)
  4. PSA

Sonography

  1. Quantification of residual urine after micturition
  2. Renal ultrasound
  3. Quantification of leaked urine: pad test

Additional testing

  1. Micturition cysto-urethrogram
  2. Urodynamic examination to measure bladder pressure
  3. Cystoscopy – to rule out tumours
  4. MRI to identify pelvic floor defects
83
Q

Treatment for urinary incontinence

A

Physical measures to prevent leakage

  • Absorbent products
  • Catheterisation
  • Urethral occlusion
  • Pessaries and penile compression devices

Lifestyle changes

  • Weight loss
  • Dietary changes (e.g. decrease consumption of alcohol, caffeine, carbonated drinks)
  • Smoking cessation

Behavioural therapies and exercise

  • Bladder training
  • Kegal exercises
  • Vaginal weighted cones
  • Biofeedback

Medical treatment (urge incontinence)

  1. Anticholinergics (oxybutynin) – competitive blockage of acetylcholine at the muscuranic acetylcholine receptors -parasympathetic receptors - parasympathetic effect is impaired - decreased overactivity of the detrusor muscle - reduced voiding
  2. Alternatives
  • Alpha blockers e.g. tamsulosin – useful in BPH
  • Additional spasmolytic agents e.g. scopolamine – reduce bladder spasms
  • Tricyclic antidepressants (anticholinergic) e.g. imipramine

Topical vaginal oestrogen in postmenopausal patients with vaginal atrophy

For BPH

  1. Finasteride – Alpha-reductase inhibitor, which inhibits the production of dihydrotestosterone from testosterone. Medication may stop prostate growing.
  2. Alpha-blockers e.g. prazosin – relax smooth muscle of the prostate and bladder neck, which allows urine to flow more easily. Provide immediate benefits
  3. Transurethral prostate resection
84
Q

histological changes in diabetic nephropathy

A

Three major histological changes occur

  1. Glomerulosclerosis
  2. Glomerular basement membrane thickening
  3. Mesangial expansion
85
Q

Features of nephritic syndrome

A
  1. Azotaemia/ uraemia (elevated serum urea/ creatinine)
  2. Oliguria
  3. Haematuria (macroscopic usually)
  4. Mild to moderate proteinuria
  5. Hypertension
86
Q

Types of nephritic syndrome

A
  1. Post infectious glomerulonephritis
  2. IgA Nephropathy
  3. Mebrano-proliferative glomerulonephritis
87
Q

Features of nephrotic syndrome

A
  1. Proteinuria
  2. Hypoalbuminaemia
  3. Peripheral oedema
  4. Hyperlipidaemia
  5. Lipiduria
88
Q

Types of nephrotic syndrome

A
  1. minimial change disease
  2. membranous nephropathy
  3. focal segmental glomerulosclerosis
89
Q
A
90
Q
A