Week 9 Flashcards
The urinary tract
The uro-epithelium:
-3-5 layers thick
-impervious to urine
-from the calyx to external meatus
-urinary carcinogens
Continuous production of urine
Urine is sterile
Unidirectional flow
Stagnation, reflux and UTI
Urology in nutshell
LUTS- micturition cycle, pharmacology. OAB, BPH
Urinary incontinence- urodynamics, stress incontinence, neuropathic bladder
PSA- DRE/TRUS/MRI/prostate zones, Ca prostate
Haematuria- imaging, endoscopy, risk factor,renal and urothelial Ca
Pain- imaging, stone aetiology, urinary stones, scrotal pathology
Dysuria- microbiology, UTI
Retention- catheterisation, causes acute/chronic retention
Lumps- inguino scrotal anatomy, scrotal lumps, hernia, torsion, testicular tumours
Erectile dysfunction infertility- physiology of erection, sperm physiology, andrology
LUTS
Storage symptoms:
-day frequency
-night frequency
-urgency
-incontinence
— urge
—stress
—overflow
—anatomical
Voiding symptoms
-hesitancy
-poor stream
-terminal dribbling
-post micturition dribbling
Micturition cycle
Bladder filling:
-detrusor muscle relaxes, urethral sphincter tone, pelvic floor tone
first sensation to void:
-detrusor muscle relaxed
-urethral sphincter contracts
-pelvic floor contracts
Normal desire to void:
-detrusor muscle contacts
-urethral sphincter relaxes (voluntary control)
-pelvic floor relaxes
-micturition
Bladder filling:
-detrusor muscle relaxes
-urethral sphincter tone
-pelvic floor tone
Assessment of LUTS
Essential
-symptom questionnaires
-MSU
-U/E ?PSA
-bladder scan
-frequency/vol chart
Optional:
-flow rate
-plain X-ray KUB
-USS renal tract/CT
-urodynamics
-cystoscopy
Examination
Abdominal examination
-suprapubic tenderness
-palpable bladder
-consistency
-shape
-abnormalities
Genitalia examination
Digital rectal examination/vaginal exam
Flow rates
Maximum and mean flow rates decrease with age
Flow rates between 10 and 15 mls/sec may be normal over 70 years of age
>15mls/sec normal
10-15 mls/sec-equivocal
<10mls/sec-obstructed
Causes of voiding dysfunction
UTI
Overactive bladder
Bladder outlet obstruction
Bladder cancer
Prostate cancer
Gynaecological problems
Bladder stones
Fistulas
Management of LUTS
Conservative
Medical therapy: alpha blocker/ 5 alpha reductase inhibitors, anti cholinergic
Surgical treatment:
-urolift
-rezum/steam therapy
-TURP/green light laser prostatectomy
-holmium laser enucleation of prostate
-open/robotic prostatectomy
Urinary incontinence
Types of incontinence:
-overflow: urethral blockage, bladder unable to empty properly
-stress: relaxed pelvic floor, increased abdominal pressure
- urge: bladder over sensitivity from infection, neurologic disorders
Causes of urinary incontinence
Genuine stress incontinence- congenital weakness of bladder neck, denervation of sphincter mechanism of pelvic floor (during delivery), oestrogen deficiency in menopause etc
Detrusor instability
Retention with overflow incontinence
Urogenital fistula
Temporary- UTI, drugs-a-blockers
-urethral diverticulum
Management of urinary incontinence
Conservative
Urethral catheter for overflow incontinence
Anti cholinergic/adrenergic agonists for urge incontinence
Surgical for significant stress incontinence
-plugs, bulking agents, tapes, mesh, artificial urinary sphincters
-correction of anatomical cause
Haematuria
Visible Haematuria
Non-visible Haematuria
-symptomatic
-asymptomatic
Haematuria investigations
FBC/ U&E, MSU— essential
Urine cytology/ blood PSA in men
CT urogram
Other imaging: USS; retrograde pyelogram; MRI
Endoscopy: essential flexible/rigid cystoscopy; ureteroscopy
Rarely biopsy
Bladder cancer classification
G1, G2, G3, CIS
PTa, pT1, pT2, pT3, pT4
Low risk: TURBT mitomycin C X1
Medium risk: mitomycin C X6
High risk: BCG therapy/radical cystectomy
Muscle invasive: radical cystectomy or radiotherapy
Bladder cancer outcomes
Superficial:
-70% remain superficial and have an excellent outcome
-30% can become invasive and their outcome depends on the treatment offered
Invasive:
-surgery 60% 5 yr survival
-radiotherapy 40% 5 yr survival
renal cancer
May not present with Haematuria
May be incidentally discovered on USS or CT
Tumour types:
-renal parenchyma (Renal cell ca) more common
-collecting system TCC
-other rare types
Renal cancer evaluation
Solid/cystic
-if cystic-> characters
-if solid-> is it malignant
Other kidney conditions
Baseline renal function
Any signs of advanced disease
Any metastasis
PSA
Prostatic specific antigen
Protease enzyme secreted in the seminal fluid
Small amounts gets to blood stream during cell division
Bound tightly to plasma proteins
Raised in blood stream:
-enlarged prostate
-prostatitis
-ca prostate,
-all these conditions can have normal PSA
Age specific ranges (oesterling)
40-49 years- 2.5
50-59- 3.5
60-69- 4.5
70 > -6.5
Prostate cancer
Asymptomatic
Raised PSA/abnormal DRE
LUTS
Backache
Symptoms of metastasis
Symptoms of local progression
Diagnosis:
-PSA
-TRUS biopsy
-TURP
Staging:
-DRE
-bone scan
-CT/MRI
Retention of urine
Acute
-painful
-residual Vol 1<1000ml
-relief on catheterisation
Chronic retention;
-usually painless
-usually residual vol >1000ml
2 types:
-low pressure
-high pressure: back-pressure effects on kidney
Management of retention
Check bloods before catheterisation
Type and size of catheter
Record residual volume
If chronic renal failure then closely monitor urinary output
Plan TWOC or definitive surgery
Physiology of micturition
Bladder wall parasympathetic
Urethral sphincter voluntary- pudendal
Storage: BW relaxed, US contacted/tonic
Voiding: BW contracted, sustained, US relaxed
Red flag signs and symptoms
Abnormal PSA/DRE
Haematuria
Renal mass (palpable or on scan)
Testicular mass (palpable or on scan)
Penile lump/discharge
Reciprocal induction
Day 32- ureteric bud (metanephric duct) sprouts into intermediate mesoderm- metanephric blastema
The ureteric bud bifurcates repeatedly- each bifurcation capped with mesoderm which eventually give foetal kidney its lobulated appearance
The ureteric bud and kidney rely on signals from each other to keep developing (an example of reciprocal induction) ie in the absence of one the other will regress
The metanephric duct gives rise to collecting ducts and the metanephric bastema the rest of the nephron
Urine production begins at about week 10 when all tubules have finally canalised and joined together
Ureteric bud division ceases about week 15 where a nephrons continue to develop to week 36
What is the prostate
Small walnut sized gland found in men
Produces and secretes fluid which nourishes sperm
-proteolytic enzymes, prostatic acid and phosphatase, fibrinolysin, zinc, PSA (prostate-specific antigen)
Lobes of prostate gland
Anterior lobe
Median lobe
Lateral lobes
Posterior lobe
Prostate zones
“McNeal” zone
Peripheral zone: < 70% glandular tissue, origin 70-80% prostate cancers
Central zone: 25% glandular tissue, origin <5% of prostate cancers surrounds ejaculatory ducts
Transition zone: 10% glandular tissue, origin of benign prostatic hyperplasia
Anterior fibromuscular stroma: ~5%, no glandular components
Diseases of prostate
Surgical sieve
Vascular
Infection/inflammation
Traumatic
Autoimmune
Metabolic
Idiopathic/iatrogenic
Neoplastic
Degenerative
Most common prostate diseases:
-prostatitis
-benign prostatic enlargement
—lower urinary tract symptoms
—urinary retention
-prostate cancer
Benign prostatic enlargement
By age 65, 50% men will experience BPE
-at age of 90, 90% of men will have BPE
Benign increase in the number of epithelial and stroma cells in the transition zone
BPE is a clinical diagnosis
-LUTS, DRE, uroflowmetry, imaging
Benign prostatic hyperplasia is a histological diagnosis, has to be proven at biopsy
Symptoms not always proportional to degree of BPE
May present with urinary retention
Lower urinary tract symptoms LUTS
Storage symptoms:
-frequency
-urgency
-urge incontinence
-nocturia
-nocturnal enuresis (bedwetting)
-incomplete emptying
Voiding symptoms:
-haematuria- red flag symptom
-dysuria
-hesitancy
-poor flow
-intermittent stream
-spraying/splitting of stream
-terminal dribbling
BPE-investigations
Uroflowmetry (“flow studies”)
Post-void residual
PSA and renal function
Urine dipstick testing +/- urine MC&S
Bladder diary
Urodynamics, USS KUB may be necessary
BPE-medical management
Alpha 1 adrenoceptor antagonist:
-tamsulosin
-inhibits effect of noradrenaline on smooth muscle in the prostate and bladder neck, relaxing smooth muscle and relieving obstructive symptoms
-Hours/days full effect within weeks
-retrograde ejaculation, dizziness, postural hypotension (take medications before bed), floppy iris syndrome during cataract surgery
5alpha reductase inhibitor:
-finasteride, dutasteride
-inhibits conversion of testosterone to dihydrotestosterone- more potent form drive hyperplasia works to shrink gland
-6weeks-6months
-erectile dysfunction, reduced libido, gynaecomastia (1-2%) doesn’t resolve with stopping medication, ejaculation disorders
BPE-medical management
Watchful waiting- not all men require treatment
Combination therapy (tamsulosin and finasteride) more effective than monotherapy
Surgical management
Transurethral resection of prostate (TURP)
Holmium laser enucleation of the prostate (HoLEP)
Greenlight laser prostatectomy
Prostatic urethral lift
Open prostatectomy
Aquablation (Rezum )
Urinary retention types
Acute urinary retention: the acute and painful inability to pass urine which is relived by insertion of catheter
-immediate management: 2 way 14-16Fr urethral catheter
-document residual volume, colour of urine, easy or difficult passage
Chronic urinary retention: adapting to distal obstruction, low pressure, high pressure HPCR
-over time the bladder stretches and capacity increases
-often painless
-large residual volume >800ml
-renal impairment/hydronephrosis
-decompression haematuria
-post obstructive diuresis
Causes of urinary retention
Inflammatory: UTI, prostatitis
Obstructive: BPE, stricture, bladder neck stenosis, constipation, pelvic mass, clot retention
Drugs: alcohol, diuretics, spinal/epidural anaesthesia, opioids
Neurogenic: cauda equina syndrome CES, spinal cord injury, MS, Parkinson’s disease, pelvic injury/trauma, pelvic surgery
Urinary retention
Red flag symptoms:
-low back pain, lower limb neurology, saddle anaesthesia-> think cauda equina syndrome- full neuro exam
-weight loss, bony pain, haematuria -> think malignancy
-nocturnal bedwetting indicative of HPCR
Examination:
-abdomen- has pain and abdominal swelling resolved
-DRE- is prostate enlarged, smooth, craggy, hard, nodules, tender, blood, faecal loading, anal tone, saddle anaesthesia
Investigations:
- urine MC&S, FBC, UE (urea and electrolytes), CRP (if infection)
Management: treat the cause
-hourly UO monitoring
—post obstructive diuresis indicates HPCR
—if UO >150ml/hr over 2 consecutive hours
—Normal saline (0.9% NaCl) replacement of half that volume over the following hour
-tamsulosin 400mg trial without catheter
If HPCR do not remove catheter
-options: long term catheter, intermittent self-catheterisation, surgery ie TURP
Prostatitis
Causative pathogen detected in only 10%
-acute bacterial prostatitis -E.coli
-chronic prostatitis (>3 months symptoms)- wider spectrum
-immunosuppressed states- TB, candida
Risk factors: UTI/epididymitis , transurethral surgery, indwelling catheter, immunosuppression
History: fevers, rigors, general malaise, perineal pain, LUTS
May present as AUR or recurrent UTIs
Examination: suprapubic tenderness, palpable bladder
-DRE: tender, “boggy” prostate, fluctuance suggests abscess
Investigations: urine dip, FBC, UE, CRP, lactate
-post void bladder scan to assess residual urine
-mid stream urine for culture
-blood culture if febrile
Management:
-may be septic-> resuscitation with A to E
-Sepsis 6
Antibiotic choice guided by local protocols and previous sensitivities
-often broad spectrum penicillin +/or quinolone (ciprofloxacin)
-consider extended oral course on discharge
Prostate cancer presentation
Prostate adenocarcinoma is the most common cancer in men in uk
Signs and symptoms:
-may be asymptomatic opportunistic PSA testing
-LUTS
-haematuria, haematospermia
-abnormal DRE (hard, nodular, craggy prostate, asymmetry)
Advanced disease:
-leg swelling, anorexia, weight loss, bony pain, coagulopathy, neurological defects
Risk factors:
-age, ethnicity, family history, BRCA2 gene mutations
Prostate cancer- evaluation
PSA- prostate specific antigen
-enzyme produced by the prostate to liquefy semen
- raised serum PSA in UTI, prostatitis, urinary retention, urethral instrumentation incl, catheterisation, ejaculation, BPE and cancer
-age specific “normal” ranges
-must be corroborated with history, examination and DRE
MRI of prostate- diagnosis and local staging
TRUS biopsy (transrectal ultrasound guided prostate biopsy)
Or transperineal prostate biopsy
Gleason grading system:
-cells are graded 1-5 (5 most abnormal)
-the most common and second most common grades are noted and added together
-Gleason 4+3 is more abnormal than 3+4
Prostate cancer staging
T1: non palpable disease
T2: palpable confined prostate
T3: spreads outside prostate
T4: adjacent organs involved
N: lymph node spread
M: non regional lymph node spread
MRI: T, N
Nuclear medicine bone scan- M
CT TAP (thorax, abdo, pelvis)- N, M
Prostate cancer management
All patients should be discussed in urology MDT
Active surveillance:
-aim is to avoid treating indolent cancers by only treating if sign of progression
-suitable if medically fit, life expectancy> 10-15 years, localised disease
-regular monitoring PSA +DRE look for evidence progression
Watchful waiting: not fit for curative treatment
-suitable if life expectancy<10-15 years, significant comorbidities therefore not fit for radical treatment
-avoiding treatment unless patient develops symptoms
-disease control rather than cure
Prostate cancer- management types
Radiotherapy: is suitable for local and locally advanced cancer, symptomatic relief of painful bony metastases
Surgery: radical prostatectomy (open, laparoscopic, robotic) with or without lymphadenopathy
Hormone treatment: can be used for locally advanced or metastatic disease
Chemotherapy: used in metastatic disease, especially those who become resistant to hormone treatment
Role of cancer nurse specialist is vital
Shock definition
“Failure of the circulation to deliver oxygenated blood to meet tissue requirements”
Does shock matter
A reduction in blood flow to tissues depriving them of oxygen (ischaemia)
Organs of vital importance, brain, heart, and kidneys can suffer irreversible damage, eventually leading to death
Inadequate cellular oxygen delivery-> anaerobic metabolism—> inadequate energy production and lactic acid production—> metabolic failure and metabolic acidosis—> cell death
How to measure degrees of shock
Lactate levels
Measure in arterial blood gas
Urinary catheter- 0.5mls/kg. 30-40mls/hr
What determines how much oxygen gets to the tissue
Amount of oxygen in the blood
-ie (oxygen content of blood both dissolved and carried by Hb)
-the flow of blood around the circulation ie (CO)
Oxygen delivery
DO2= CO x (Hbx SPO2 x1.34) + (PaO2 x 0.2)
Oxygen carrying capacity
Increase fraction of inspired oxygen they breathe in will optimise oxygen delivery
Hb- direct measure: reduced with haemorrhage, increased with blood transfusion
O2- oxygen saturation (direct measure), dissolved oxygen. All patients in shock should get high flow oxygen
What determines cardiac output
Is the volume of blood ejected from left ventricle in a minute
CO= stroke volume x heart rate = 5L/min
SV (is the volume ejected each heart beat):
-preload (EDV)
-myocardial contractility
-afterload- (pressure the heart must work against to eject blood during systole) systemic vascular resistance
Shock preload, inotropy, afterload
Preload- Hypovolaemic: haemorrhage
Inotropy- cardiogenic: CHF, ACS, dysrhythmia, valve, cardiac tamponade
Afterload- distributive: sepsis, thryotoxicosis, anaphylaxis, neurogenic
MAP= (SV xHR) xSVR
What could be causing shock in our trauma patient
Reduced venous return
Impaired cardiac function
Reduced vascular tone- unable to vasoconstrict
Body has compensatory mechanisms to maintain oxygen delivery to essential organs
Why a high respiratory rate
Reduced delivery of oxygen
Increased anaerobic metabolism
Increased lactic acid production
Fall in arterial pH
Stimulation of peripheral chemoreceptors: carotid bodies (Glossopharyngeal nerve), aortic bodies (vagus nerve)
Respiratory centre (medulla)
Respiratory muscles: increased depth and increased rate of
Other symptoms of shock
High heart rate
Clammy skin
Cold peripheries
Pale skin
Poor capillary refill
Reduced urine output
Why do you get a reduced urine output
Renin-angiotensin- aldosterone pathway
Juxtaglomerular cells in the kidney respond to a reduction in blood volume
Renin released into blood
Angiotensinogen-> angiotensin I—ACE—> angiotensin II
Vasoconstriction, thirst, adrenal cortex (releasing aldosterone)
Vasoconstriction— increase blood pressure,
Thirst increases blood volume
Aldosterone make kidneys increase Na+ reabsorption from filtrate increase blood volume
Increase in blood volume increases blood pressure
ADH and urine output
Reduced blood flow to pituitary
Secretes ADH
Capillary ADH secreted into nephron water moves into capillary
ADH increases amount water reabsorbed from filtrate into blood
Urine output is reduced as more water is returned to the blood
Treatment
Therefore to:
-recognise shock
-treats underlying cause
-support the body in maintaining oxygen delivery to tissues
