Renal/urology Flashcards
1
Q
What is the function of the urinary tract?
A
To collect urine produced continuously by the kidneys
To store collected urine safely
To expel urine when socially acceptable
2
Q
What are the ureters?
A
25cm – 30cm
Retroperitoneal organs
Run over psoas muscle, cross the iliac vessels at the pelvic brim and insert into trigone of bladder
Urine produced by the kidney enters the renal pelvis and is transported via peristalsis down the ureter into the bladder
Reflux of urine is prevented by a valvular mechanism at the vesicoureteric junction
3
Q
What is the nervous control of the Bladder and Sphincter?
A
- Parasympathetic Nerve (pelvic nerve) comes from roots S2-S4, uses acetylcholine neurotransmitter, mediates involuntary control.
- Sympathetic Nerves (hypogastric plexus) comes from roots T11 – L2, uses noradrenaline neurotransmitter, mediated involuntary control.
- Somatic Nerve (pudendal nerve) comes from roots S2-S4, sends info “viaOnuf’s nucleus”, uses acetylcholine neurotransmitter
- Afferent pelvic nerve (sensory nerve), sends signals from detrusor muscle
4
Q
How are centres/nuclei in the brain involved with micturition?
A
Cortex: voluntary control
Pontine Micturition Centre/Periaqueductal Grey: Co-ordination of voiding
Sacral Micturition Centre: Micturition reflex
Onuf’s Nucleus: Guarding reflex
5
Q
What is the storage phase in urophysiology?
A
Bladder fills continuously as urine is produced by kidney and is passed through the ureters into the bladder
Normal adult bladder capacity 400-500ml with first sensation at 100-200ml
As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance
6
Q
What is the filling phase in urophysiology?
A
At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation Somatic (Pudendal) nerve stimulation maintains urethral contraction
7
Q
What happens during the voiding phase (aka Micturition reflex)?
A
Micturition reflex is an autonomic spinal reflex
Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord
Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts
Pudendal nerve is inhibited and the external sphincter relaxes
8
Q
How does the bladder empty?
A
Coordinated detrusor contraction with external sphincter relaxation to expel urine from bladder
A positive feedback loop is generated until all urine is expelled
Detrusor relaxation and external sphincter contraction after complete emptying of bladder
9
Q
What is the guarding reflex?
A
Voluntary control of micturition can occur in anatomically and functionally normal adults.
Afferent signals from the pelvic nerve are received by the pontine micturition centre/periaqueductal gray and transmitted to higher cortical centres.
If voiding is inappropriate the guarding reflex occurs.
Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation.
Pudendal nerve stimulation results in contraction of the external urethral sphincter.
10
Q
What muscular changes occur between storage and micturition?
A
STORAGE
Receptive Relaxation
Detrusor relaxation (sympathetic stimulation T11-L2)
External Urethral Sphincter contracted (pudendal stimulation S2-4)
MICTURITION
Voluntary control from cortex and pontine micturition centre
Detrusor contraction (parasympathetic stimulation S2-4)
External Urethral Sphincter relaxation (pudendal inhibition S2-4)
11
Q
What is the normal function of the lower urinary tract?
A
Convert a continuous process of excretion (urine production) to an intermittent process of elimination.
Store urine insensibly
Void urine when convenient
12
Q
What muscular systems are involved in the lower urinary tract?
A
- Detrusor muscle Relaxes during storage (compliant) Contracts during voiding - Distal sphincter mechanism Contracts during storage Relaxes during voiding
13
Q
What is the neural control of the lower urinary tract?
A
- Parasympathetic (Cholinergic) S3-5 Drive detrusor contraction - Sympathetic (Noradrenergic) T10-L2 Sphincter/urethral contraction Inhibits detrusor contraction
14
Q
What are Lower urinary tract symptoms (LUTS)?
A
STORAGE symptoms Frequency Nocturia Urgency Urgency Incontinence
VOIDING symptoms Hesitancy Straining Poor/intermittent stream Incomplete emptying Post micturition dribbling Haematuria Dysuria
15
Q
What is BPH, BPE, BOO and LUTS?
A
BPH – benign prostatic hyperplasia (histological)
BPE – benign prostatic enlargement (DRE findings)
BOO – bladder outflow obstruction (urodynamic proven obstruction)
LUTS - Lower urinary tract symptoms, a constellation of symptoms, neither gender nor disease specific
16
Q
What is benign prostatic hyperplasia?
A
Increase in epithelial and stromal cell numbers in the periurethral area of the prostate.
May be due to increase in cell number
Or due to decrease apoptosis
Or due to combination of the two
17
Q
What are the two aspects that lead to benign prostatic obstruction?
A
Alpha1 adrenoceptor mediated prostatic smooth muscle contraction (dynamic). Smooth muscle accounts for 40% of the area density of the hyperplastic prostate
Volume effect of BPE (static)
18
Q
What is the link between Androgens and BPH?
A
Androgens do not cause BPE, but are a requirement for BPH
Castration prior to puberty or genetic diseases that inhibit androgen action or production, men do not develop BPH
Androgen withdrawal leads to partial involution of established BPH
19
Q
How take a history for LUTS?
A
What symptoms? storage, voiding or mixture Duration of symptoms Past medical history Past surgical history Drug history Allergies Symptom scoring e.g. IPSS Bother (often incorporated as part of symptom score) -establish symptoms that are most bothersome to the patient
20
Q
What is the IPSS?
A
International Prostate Symptom Score (IPSS)
Used to assess severity of symptoms in benign prostatic hypertrophy
21
Q
What examinations might you do for LUTS?
A
General examination i.e fitness for surgery Abdominal examination External genitalia Digital rectal examination (DRE) Focussed neurological examination Urinalysis
22
Q
What investigations might you do for LUTS?
A
Renal biochemistry Imaging PSA? Flow rates and residual volume Frequency volume chart TRUSS – trans-rectal ultrasound scan (for size) Flexible cystoscopy (if infection, stones, haematuria or recent onset storage symptoms) Urodynamics
23
Q
What are normal flow rates for men?
A
Men < 40 >= 21 ml/s
Men 40-60 >= 18 ml/s
Men > 60 >= 13 ml/s
Need to void at least 125mls of urine for representative flow
24
Q
When might flow rates be reduced?
A
Flow rates can be reduced due to obstruction within the lower urinary tract
They can also be reduced due to detrusor underactivity (pump failure)
25
What is Post Void Residual (PVR)?
The amount of urine retained in the bladder after a voluntary void and functions as a diagnostic tool.
Typically performed using ultrasound, a bladder scanner, or with a urinary catheter.
100% normal men have PVR < 12 ml
Consider detrusor underactivity as cause of high PVR
26
How does the flow rate indicate obstruction?
Qmax >15ml/s - 24% obstructed
Qmax 10-15ml/s - 54% obstructed
Qmax <10ml/s - 88% obstructed
27
What are the complications of benign prostatic enlargement?
```
Symptom progression (17-40%)
Infections (0.1-12%)
Stones (0.3-3.4%)
Haematuria
Acute retention (1-2% per year)
Chronic retention
Interactive obstructive uropathy (<2.5%)
```
28
What is Acute retention of urine (AUR)?
Painful
Typically 600-1L residual urine
Normal U&E’s
Pain relieved by catheterisation
Precipitated retention – often does not recur
Spontaneous retention – 50% recur very early, 70% within a year
Treatment:
Alpha-blockers have a role in trial without catheterisation (TWOC)
Intermittent self-catheterisation
Bladder outflow surgery
29
What is chronic retention of urine?
More difficult to define
Incomplete bladder emptying
Increased risk of infections and stones
Can be low pressure with detrusor failure
Can be high pressure, with risk of interactive obstructive uropathy
30
What is Interactive obstructive uropathy?
A structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction.
Nocturnal enuresis should be warning sign
Residual volume can be up to 4L
Check U&Es and monitor daily if creatinine raised, check BP
Observe for a diuresis (excessive production of urine)
Long term options:
Transurethral resection of the prostate (TURP) or indwelling catheter
31
What is nocturnal enuresis?
Nocturnal enuresis is involuntary urination that happens at night while sleeping, after the age when a person should be able to control his or her bladder. (Involuntary urination that happens during the day is known as diurnal enuresis.)
32
What are the treatment aims for LUTS?
Improve urinary symptoms
Improve quality of life
Reduce complications of bladder outflow obstruction
33
When might you suggest watchful waiting for men with LUTS?
Suitable for men with mild symptoms
Over 5 years 25% progress, just under half remain static and 30% improve, 2% experience acute retention
Lifestyle changes may be useful
34
What's the treatment for BPE?
Aimed at either reducing the prostatic smooth muscle tone or reducing size of the prostate
Alpha – adrenergic antagonists, (e.g. Alfuzasin XL, Tamsulosin), improves flow average 3ml/s
5-alpha-reductase inhibitors, (e.g. Finasteride, dutasteride) inhibit the conversion of testosterone to the more active, dihydrotestosterone, reduces size 20-30%
Combination therapy better than either singly
Anti-cholinergics for overactivity
35
When would a patient with LUTS need surgery?
```
RUSHES
Retention
UTI’s
Stones
Haematuria (that isn't responding to 5-ARI)
Elevated creatinine due to BOO
Symptom deterioration
```
36
What are the surgical treatment options for BPE?
```
Bladder neck incision
Trans-urethral resection of prostate (TURP)
Bipolar
Greenlight laser
Thullium laser
Holmium enucleation
Millins retro-pubic prostatectomy
```
37
What are the potential complications of TURP?
Immediate – Sepsis, haemorrhage, TUR syndrome
Early – Sepsis, haemorrhage and clot retention
Late - Retrograde ejaculation, erectile dysfunction, urethral stricture, bladder neck stenosis, urinary incontinence
38
Why are the symptoms of LUTS different between the genders?
Women have a very weak sphincter mechanism, especially after childbirth. Get stress incontinence more commonly, less problems with passing urine.
Men have quite tight sphincter mechanisms, more problems with passing urine.
39
What are the basic centres involved in neuro-urology?
- Cortex - in control of sensation and voluntary initiation
- PMC/PAG - involved in coordination and completion of voiding
- Spinal reflexes - involved in reflex bladder contraction (sacral micturition centre), guarding reflex (Onaf’s nucleus), receptive relaxation (sympathetic)
40
How is the lower urinary tract controlled by the nervous system?
During the storage phase the internal urethral sphincter remains tense and the detrusor muscle relaxed by sympathetic stimulation. During micturition, parasympathetic stimulation causes the detrusor muscle to contract and the internal urethral sphincter to relax. The external urethral sphincter (sphincter urethrae) is under somatic control and is consciously relaxed during micturition.
Central coordination from the pontine micturition centre
41
What happens in normal bladder function?
Storage (99%)
Sympathetic causes detrusor relaxation and sphincter contraction.
Bladder fullness increases, messages to the pons and higher centres to consider voiding.
Can be postponed until it is convenient.
Voiding (1%)
PMC co-ordinates voiding via parasympathetic, causes detrusor contraction and sphincter relaxation at the same time.
42
How are LUTS classified?
Storage - frequency, urgency, nocturia (waking up to urinate with the intention of going back to sleep), incontinence
Voiding - slow stream, splitting or spraying, intermittency (some flow, no flow), hesitancy (takes a while to get started), straining, terminal dribble
Post-micturition - post-micturition dribble, feeling of incomplete emptying
43
What are the parameters used in a bladder diary?
Parameters - frequency per day (2-8) and per night (0-1), volume per day (2L) and per night (900ml), nocturnal volume (20% young, 33% elderly), functional capacity (>400ml) and incontinence per day (0)
Normals in brackets.
44
What are the different types of incontinence?
Urgency incontinence - associated with an urgent desire to void which is difficult to defer
Stress incontinence - associated with increase in abdominal pressure due to coughing/straining
Mixed incontinence - combination of stress and urgency
Continuous incontinence - due to a fistula
Overflow incontinence - occurs in the presence of a full bladder
Social incontinence - occurs in those with dementia
45
What is an overactive bladder?
OAB is defined as urgency with frequency with or without nocturia when appearing in the absence of local pathology.
Can be wet or dry
Detrusor overactivity may be seen on urodynamics (measures bladder pressure)
46
How is an overactive bladder managed?
Behavioural therapy - frequency volume chart, caffeine, alcohol, bladder drill
Antimuscarinic agents - decrease parasympathetic activity by blocking M2/M3 receptors but have side-effects of a dry mouth
B3 agonist - increase sympathetic activity at B3 receptor in bladder
Botox - blocks neuromuscular junction for ACh release, side effects of incomplete bladder emptying (need to catheterise in 15%)
Sacral neuromodulation - insertion of electrode to S3 nerve root to modulate afferent signals from bladder (pacemaker battery tells it to relax)
Surgery - augmentation cystoplasty, involves major surgery
47
What causes stress incontinence in females?
Usually secondary to birth trauma
- denervation of the pelvic floor and urethral sphincter
- weakening of fascial support of bladder and urethra
Neurogenic
Congenital
48
How do you treat stress incontinence in females?
Pelvic floor physiotherapy
Can use Duloxetine to increase contraction of urinary sphincter (but does have side effects)
Surgery
49
What causes stress incontinence in males?
Neurogenic
| Iatrogenic (prostatectomy)
50
How would you treat stress incontinence in males?
Treat with artificial urinary sphincter or male sling
51
What causes voiding problems and how would you treat them?
Obstructive - BPE, urethral stricture, prolapse/mass
If BPE - give alpha blockers with or without 5alpha reductase inhibitor. Another option is PDE5i with erectile dysfunction. If the above fails then use TURP.
Non-obstructive - detrusor underactivity
Long term catheterisation to empty - ISC/LTC/SPC
Sacral neuromodulation in trial phase-works in Fowlers syndrome
52
What are the features of a Spastic spinal cord injury (supra-conal lesion)?
```
If there is a lesion above the cauda equina, the brain is no longer connected to the lower body (upper motor neuron lesion).
Bladder over-contracting.
Loss of coordination and completion of voiding.
Features:
- Reflex bladder contractions
- Detrusor sphincter dyssynergia
- Poorly sustained bladder contraction
- Potentially unsafe bladder
```
53
What are the features of a Flaccid Spinal cord injury (conus lesion, decentralised bladder)?
```
Lesion at the level of the cauda equina.
Bladder never contracts.
Features:
- Areflexic bladder
- Stress incontinence
- Risk of poor compliance
- Loss of Guarding reflex
- Loss of Receptive relaxation
```
54
What is an unsafe bladder?
One that puts the kidneys at risk due to raised bladder pressure
Causes: prolonged detrusor contraction or loss of compliance
Result: problems with drainage of urine from the kidneys and ultimately hydronephrosis and renal failure
55
What is Autonomic Dysreflexia?
Occurs lesions above T6
Overstimulation of sympathetic nervous system below level of lesion in response to a noxious stimulus.
Symptoms: Headache, severe hypertension, flushing.
56
What are the aims for managing a neurogenic bladder?
Bladder safety
Continence/symptom control
Prevent autonomic dysreflexia
57
How to treat an unsafe bladder?
Harness reflexes to empty bladder into incontinence device (may not keep bladder safe)
OR
Suppress reflexes converting bladder to flacid type and then empty regularly
58
How to manage the bladder in a paraplegic?
Suprapubic catheter
Convene drainage
OR
Suppress reflexes or poorly compliant bladder converting bladder to safe type and then emptying regularly using ISC
59
What is convene drainage?
A sheath that allows for urine to be funnelled away from your body and stored in a discreet bag secured comfortably to your leg.
No indwelling catheter
Needs monitoring
Develop incomplete bladder emptying long term
60
What is a supra-pubic catheter?
An SPC is inserted a couple of inches below your navel, , directly into your bladder, just above your pubic bone. This allows urine to be drained without having a tube going through your genital area.
Inserted under anaesthetic
Risk of infections, stones and autonomic Dysreflexia if blocked
61
How would you treat Neurogenic stress incontinence in men and women?
Ensure that bladder is safe before treating
Men: artificial sphincter
Women: autologous sling, artificial sphincter, synthetic tapes (TVT/TOE) - not recommended by NICE
62
What bladder problems are frequently found in patients with MS?
Overactive bladder syndrome - urinary urgency and frequency, caused by neurogenic detrusor overactivity
Incomplete bladder emptying
63
What are the risk factors for prostate cancer?
Age - 100% of prostates at 80 years old
Family history - 2-3x increased risk if first degree relative is affected
Ethnicity - 50% more PC in afro-carribean patients
Genetic - more common in younger patients
64
What are the different areas that prostate cancer can occur?
```
Majority is adenocarcinoma
Site:
Peripheral zone (70%)
Transitional zone (20%)
Central zone (10%
Cases in the transitional and central zone are difficult to palpate in a digital rectal exam.
```
65
How are prostate cancers graded?
Gleason grading system used. Correlation between Gleason grade and biological behaviour of the tumour.
Gleason established five grades of glandular morphology. The two most prominent glandular patterns are graded from 1 to 5. The sum of these two grades will range from 2-10, with 2 representing the most differentiated, and 10 the most undifferentiated.
Take 2 most common patterns in the biopsy, added together and then calculate the gleason score.
66
Where can the prostate cancer spread to?
Lymphatics - to the external iliac )obturator group), internal iliac and presacral node. Occasionally , the supraclavicular nodes are involved via the thoracic duct.
Blood vessels
Directly into the bladder, seminal vesicles
Lung, thyroid, kidney, breast and prostate most commonly metastasise to the bone.
67
How might you stage a prostate cancer using TNM?
T1 Clinically inapparent tumour neither palpable or visible by staging
T2 Tumour confined within the prostate
T3 Tumour extends through the prostate capsule
T4 Tumour is fixed or has invaded adjacent structures
N1 Metastasis in regional lymph nodes
M1 Distant metastasis - can split into categories depending on where it has spread
68
How might prostate cancer present?
Weight loss
Fatigue
Loss of appetite
Night sweats
Difficulty urinating - hestinancy, slow stream, post-micturition dribble
Bone pain
Neurological deficits from spinal cord compression
Lower extremity pain and oedema
Uremic symptoms can occur from ureteric obstruction
69
What would you expect in an examination for potential prostate exam?
DRE: a nodule, asymmetry, difference in texture and bogginess
Neurologic examination, including determination of external anal sphincter tone, should be performed to help detect possible spinal cord compression.
Overdistended bladder due to outlet obstruction
Bony tenderness
70
What is the PSA test?
PSA
A glycoprotein produced only by prostate cells. Thus it is specific to the prostate but not to prostate cancer.
Can be used as a screening test - high sensitivity, but low specificity
Normal level less than 3ng/ml. Elevated level suggesting prostate cancer.
71
What are the investigations you can use to assess whether it is prostate cancer or not?
- PSA test
- MRI Prostate: Most centres perform this prior to a biopsy to identify lesions to target with biopsy. Also aids in local staging.
- Prostate biopsy: Indications - a palpably suspicious DRE regardless of PSA level, PSA >3.0ng/mL, suspicious lesion on MRI, TRUE or transperineal
- Staging imaging: Use in higher risk patients based on PSA, clinical stage and Gleason grade
- To look for evidence of nodes or metastatic disease use a bone scan orCT abdomen
72
What are the treatment options for prostate cancer?
Treatment depends on grade, stage, patient comorbidities, life expectancy and preference.
- Active surveillance: aims to minimize treatment related toxicity without compromising survival, Can only use in low risk patients.Curative treatment prompted by rising PSA.
- Radical prostatectomy: used in fit patients with localised cancer. Complication include urinary incontinence and impotence.
- Radiotherapy: used in localized and locally advanced cancer. Can cause impotence and urinary problems.
73
What are the treatment options for metastatic prostate cancer?
```
Hormone therapy
Chemotherapy
Bisphosphonates
Radiotherapy for bone pain
TURP to relieve symptoms of bladder outflow obstruction
Nephrostomies for ureteric obstruction
```
74
How can hormone therapy be used to treat prostate cancer?
Used in locally advanced or metastatic disease
Prostate cancer is androgen sensitive
May take the form of:
- Orchiectomy: a surgical procedure to remove both testicles, the main source of testerone
- LH-releasing hormone agonist e.g. leuprolide, goserelin, buserelin
- Antiandrogens block the action of testosterone e.g. flutamide, bicalutamide
Important to counsel patients on side effects - impotence, depression, hot flushes, lethargy etc
Hormone resistance can occur quickly or after a few years.
75
What is the prognosis of prostate cancer?
Localized prostate cancer - excellent prognosis with 70-90% 10 year disease-specific survival figures
Locally advanced, non-metastatic disease - median survival of 7 year
Metastatic disease - median survival of 2-3 years
Once the state of hormone-resistant disease has been reached, the median survival is 6-12 months
76
What are the risk factors for renal cancer?
Smoking - 2 fold increased risk
Environmental - petroleum, phenacetin, cadmium
Occupational - leather tanners, shoe workers, asbestos
Hormonal - obesity, diethylstilbestrol
Genetic - VHL, BHD etc
77
How might renal cancer present?
Classic triad - mass haematuria and pain (<10%)
Incidental (>50%)
Haematuria
Symptoms of metastatic disease
Paraneoplastic syndrome symptoms - PTH, erythropoietin, prolactin
Varicocele rare but do worry if it’s on the right side
78
How are renal cancers classified?
Bosniak classification
I - Benign simple cyst with thin wall without septa, calcifications, or solid component
II - Benign cyst with a few thin septa, which may contain fine calcifications or a small segment of mildly thickened calcification.
IIF - Renal cysts with multiple thin septa, a septum thicker than hairline, slightly thick wall, or with calcification, which may be thick
III - Indeterminate cystic masses with thickened irregular septa with enhancement.
IV - Malignant cystic masses with all the characteristics of category III lesions but also with enhancing soft tissue components.
79
Where might renal cancer spread?
```
Local
Nodal
Renal vein
Lungs
Bone
Brain
Pancreas
Liver
Skin
```
80
What are some of the genetic causes of renal cancer?
Von Hippel Lindau (VHL) - VHL mutation
Tuberous sclerosis - TSC 1/2 mutation
Birt Hogg Dube (BHD) - BHD mutation
Hereditary papillary RCC - C-MET mutation
81
What are the treatment options for renal cancer?
```
Surveillance (good for eldery patients with polypharmacy and comorbidities)
Radical nephrectomy (remove the entire kidney)
Partial nephrectomy
Radiofrequency ablation
Cryotherapy
Tyrosine kinase inhibitors
Cytoreductive nephrectomy
Palliative care
```
82
What are the risk factors for bladder cancer?
Smoking - 40% reduced risk after 4 year if stopped
4-aminobiphenyl broken down by N-acetyltransferase 2-polymorphic
Occupation (aromatic amines, aniline dyes and aldehydes) - tanner, rubber industry, painter, autoworker, dye worker, hairdresser, dry cleaner
Phenacetin (similar chemical structure to aniline dye)
Chronic cystitis/infection - linked with squamous cancer
LT catheter - around 10% in 10 years
Chronic HPV in immunocompromised
Pelvic irradiation - around 2-4 fold increased risk
Cyclophosphamide - due to acrolein (metabolite)
83
How might bladder cancer present?
```
Painless haematuria (no insult)
Irritative LUTS but not so specific when without haematuria
Flank pain, lower limb oedema, pelvic mass, weight loss and bone pain are uncommon but do worry if there is presentation.
```
84
What type of cancer is bladder cancer and what does it look like under a microscope?
Transitional cell carcinoma
| Microscopy - increased number of epithelial cell layers, abnormal
85
What are the risk categories for bladder cancer?
Low risk - single solitary tumour that is superficial
| High risk - high grade, intermediate, and invasive and non-invasive
86
What are the investigations for potential bladder cancer?
CT
| Cystoscopy (flexible under LA usually)
87
What are the treatment options for bladder cancer?
TURBT +/- 2nd TURBT
Intravesical chemotherapy (MMC) - inhibits DNA synthesis
Intravesical immunotherapy (BCG) - immune stimulant, upregulates cytokines
Cystectomy
Radiotherapy - high risk bladder cancer who can’t have cystectomy
Chemotherapy - cisplatin
Combination of the above
Palliative care
88
What are the risk factors for testicular cancer?
Previous TC (12 times)
Cryptorchidism
Intratubular germ cell neoplasia/testicular intraepithelial neoplasia (TIN)
Risk factors of TIN
HIV
Genetic - first degree relative (9 fold increased risk)
Maternal oestrogen exposure
89
What is the pathology of testicular cancer?
Most are germ cell tumours, divided into seminomatous and nonseminomatous
Bilateral TC are rare
Usually spread locally first into the epididymis, spermatic cord and rarely scrotal wall
90
How might testicular cancer present?
Scrotal lump - painless
Delayed presentation is not uncommon
Scrotal pain - intratumoral haemorrhage
91
What are the differential diagnosis for testicular cancer?
```
Hydrocele
Epididymal cyst
Indirect inguinal hernia
Varicocele
Testicular torsion
Acute epididymo-orchitis
```
92
How would you investigate potential testicular cancer?
Ultrasound testes - very high sensitivity
CT CAP for staging
CT brain/spine if clinically indicated
Tumour markers - AFP, LDH, hC
93
What are the treatment options for testicular cancer?
Radical inguinal orchiectomy - most definitive and diagnostic - curactive in approx 75%
Sperm banking in those without a normal contralateral testis
Biopsy of contralateral testis in those with risk factors for testicular intraepithelial neoplasia.
Others: Retroperitoneal Lymph Node Dissection (RLND), radiotherapy and chemotherapy in certain specific settings e.g. metastatic and residual tumour
94
What is Testicular intraepithelial neoplasia?
The uniform precursor of testicular germ cell tumors. ... The most common clinical situation is the case of contralateral TIN in the presence of unilateral testicular cancer.
95
What are the tumour markers for testicular cancer?
AFP - trophoblastic elements, suggestive of non-seminomatous tumour
HCG - syncytiotrophoblast elements
LDH - cellular enzymes so not overly specific but useful in follow up setting
Marks measured at presentation - good for follow up
Should be measured again at 1-2 weeks post radical inguinal orchiectomy and during follow up
96
What is Glomerulonephritis?
a group of diseases that injure the part of the kidney that filters blood (called glomeruli). Other terms you may hear used are nephritis and nephrotic syndrome. If the illness continues, the kidneys may stop working completely, resulting in kidney failure.
97
How might Glomerulonephritis clinically present?
```
Asymptomatic
Rapidly progressive glomerulonephritis (RPGN)
Chronic glomerulonephritis
Nephritic syndrome
Nephrotic syndrome
Macroscopic Haematuria
```
98
How would you diagnose Glomerulonephritis?
ANCA test is 80-90% sensitive for glomerulonephritis. About 32% of Pts with pauci-immune crescentic GN are ANCA negative, they tend to have fewer extra renal involvement.
Biopsy: Segmental glomerular necrosis with crescent formation. Degree of active lesions, fibrosis and tubular atrophy are important prognostic markers.
99
What is the epidemiology of Glomerulonephritis?
Disproportionately greater incidence in Caucasians usually during 5th, 6th or 7th decade.
100
What is the prognosis for Glomerulonephritis?
With adequate immunosuppressive treatment 5 yr renal and patient survival is 65%-75%.
Response to treatment is inversely related to creatinine concentration at the the time of initiation of therapy.
Patients with PR3 ANCA have more extra renal manifestations, higher relapse rate and higher mortality compared to Microscopic polyangiitis vasculitis patients
101
What is the treatment for Glomerulonephritis?
Induction of remission: Steroids, Cyclophosphamide. MEPEx trial- plasma exchange.
Mainatanence: CYCAZAREm trial- Azathioprine
Emerging treatments: RITUXVAS, RAVE trial - Rituximab
102
What is IgA nephropathy?
Abnormality in IgA glycosylation leads to deposition
Different to IgA vasculitis aka Henoch-Schönlein Purpura because it has extra renal manifestations.
Visible haematuria with mucosal infection.
IgA nephropathy is the most prevalent pattern of glomerular disease.
103
How would you diagnose IgA nephropathy?
Biopsy: Diffuse mesangial IgA deposits, subendothelial and sub epithelial deposits on EM is not uncommon.
104
What are the clinical features of IgA nephropathy?
Episodic macroscopic haematuria ( synpharyngitic haematuria) in 40-50% of cases in second or third of life.
Asymptomatic urine testing identifies 30-40% of cases in most reported series.
Nephrotic syndrome occurs in only 5% of all cases.
Acute kidney injurt at presentation could be due to acute tubular necrosis or crescentic glomerulonephritis.
105
How would manage IgA nephropathy?
Supportive care: BP control with RAAS inhibitors, Diet, Lower Cholesterol
Immunosuppression: Induction: Steroids, Cyclophosphamide
Remission: Steroids, Azathioprine
106
How do we classify IgA nephropathy?
Crescentic
Non-crescentic
<0.75g proteinuria - stable renal function
>0.75g proteinuria - progressive renal dysfunction
>3g proteinuria - progressive renal dysfunction
107
What is the epidemiology of Lupus in relation to glomerulonephritis?
Both Lupus and Lupus Nephritis are 3-4 times more common in African Americans, Afro-Carribeans, Hispanics and Asians.
Peak incidence is 15-45yrs with females outnumbering males by 10:1.
30%-50% pts have clinically evident renal disease at presentation.
During follow up renal involvement occurs in 60% of pts.
108
How does Lupus nephritis present?
Serology: ANCA positive, double standard DNA antibody positive. Low complement levels – C3, C4
Rash, arthralgia, kidney failure, neurological syndromes
109
How to manage Lupus nephritis?
Induction and Maintenance:
Supportive care: BP control, Diet, Lower Cholesterol
Proliferative Lupus: Good RCT evidence for Steroids, Cyclophosphamide (Euro Lupus trial: 3 months Cyclophosphamide followed by Azathioprine)
Membranous Lupus: Supportive care, Steroids, small RCT evidence for Cyclophophamide,CNIs,Azathioprine..
110
How does nephrotic syndrome present?
```
Heavy proteinuria (>3.5g/24 hours)
Hypoalvuminaemia (<30g/L)
Oedema
Hypercholesterolaemia
Haematuria usually absent or mild
```
111
What are the common causes of nephrotic syndrome?
Primary
Minimal change – children and adults
Membranous – Caucasian adults
Focal segmental glomerulosclerosis – black adults
```
Secondary
Diabetes
Amyloid (usually AL)
Infections
SLE
Drugs – gold, penicillamine
Malignancy
```
112
How would you investigate nephrotic syndrome?
Serum albumin, creatinine, lipids and glucose, urinalysis
Urine PCR
Serum and urine electrophoresis (amyloid, myeloma)
ANA, DNA Ab, C3 and C4 (lupus)
Antiphospholipase A2 receptor antibody – membranous
HepBsAg, HepCAb – Hep B or Hep C associated glomerular disease
113
How would you treat nephrotic syndrome?
Supportive – managing complications of nephrotic syndrome
Specific – treat the underlying cause
Supportive:
Control fluid state – diuretics, ACEi/ARBs, spironolactone
Statins
Anticoagulation – especially in membranous or amyloid where albumin <20g/l
114
What is membranous glomerulonephritis?
Thickening of glomerular capillary wall. IgG, complement deposit in sub epithelial surface causing leaky glomerulus.
115
What is primary and secondary membranous glomerulonephritis?
Primary: Glomerular podocyte membrane PLA2R antigen is the target antigen in 70%-80% cases of primary MN. Recent metanalysis showed 99% specificity and 78% sensitivity for PLA2R ab in diagnosing primary MN.
Secondary: Associated with Autoimmune conditions, viruses, drugs and tumours.
116
How does Membranous glomerulonephritis present?
Nephrotic syndrome and benign urinary sediment (cloudy urine)
117
How would you diagnose Membranous glomerulonephritis?
Serum PLA2R Ab and renal biopsy
118
What is the prognosis for Membranous glomerulonephritis?
30% spontaneous remission but depends on severity of proteinuria.
10yr renal survival of 100% in those who achieve complete remission, 90% with partial remission and only 45% with no remission
119
How would you manage Membranous glomerulonephritis?
Supportive treatment- control of oedema, hypertension, hyperlipidemia and proteinuria using RAS blockade, anti coagulation
Immunosuppression (steroids/ cyclophosphamide/calcineurin inhibitor)
120
What is Minimal Change disease?
Minimal change disease (MCD) is a disease where their is damage to the glomerulus. It is major cause of idiopathic nephrotic syndrome, characterized by intense proteinuria leading to edema and intravascular volume depletion.
121
How does minimal change disease present?
Nephrotic syndrome and benign urine sediment.
122
How is minimal change disease diagnosed?
Biopsy
123
What is the prognosis for minimal change disease?
MCD has a relapsing- remitting course.
MCD does not progress to renal failure. A number of adult pts with initial diagnosis of MCD are found to have focal segmental glomerulosclerosis on subsequent biopsies and they tend to have progressive renal failure.
124
How is minimal change disease managed?
Treatment: Steroids. For frequent relapses or steroid dependent cases second line treatment is with cyclophosphamide or cyclosporine.
Emerging evidence for Rituximab in the form small case series.
125
What is the physiology of an erection?
Stimulus - can be auditory or tactile
Stimulation of the cavernosal nerve with NO release
Smooth muscle relaxation - arteriole dilation and increased blood flow
Compression of venous outflow
Increased cavernosal pressure and contraction of ischiocavernosus muscle
Rigid erection
126
What is the physiology of ejaculation?
Stimulation (pudendal nerve)
Emission: peristaltic contraction of epididymis, vas deferens and seminal vesicles with simultaneous bladder neck contracture and external sphincter relaxation
Expulsion: rhythmic contraction of the bulbospongiosus muscle
127
What is erectile dysfunction?
The persistent inability to attain and maintain an erection sufficient for satisfactory sexual performance
52% of men aged 49-60
Often the first presenting symptom of cardiovascular disease
128
What are the causes of erectile dysfunction?
Endocrine - diabetes, thyroid dysfunction, hypogonadism, hyperprolactinemia
Inflammatory - prostatitis, STD
Neurogenic - CVS, MS, Parkinson’s, spinal cord injury
Pelvic surgery/trauma
Alcohol
Psychogenic - depression, anxiety, schizophrenia/bipolar
CHronic disease
Arterial disease - smoking, hypertension, PVD, hypercholesterolaemia
Medication
Obesity
129
What is non-organic erectile dysfunction?
More likely if the ED is sudden onset
Associated with relationship difficulties
Performance anxiety
Morning erections and non-coital erections generally normal
130
What should you ask about when performing a history for erectile dysfunction?
```
Onset - sudden or gradual
Duration of erections
Presence of early morning erections
Masturbation
Libido/relationship difficulties
Ejaculation dysfunction
Anatomical difficulties - physical reason (Peyronie’s disease?)
Medications
```
131
What examinations should you do for erectile dysfunction?
```
External genitalia
DRE
Full cardiovascular examination - including an ECG
Gynaecomastia (enlargement of breasts)
Neurological examination
```
132
What investigations should you do for erectile dysfunction?
```
Bloods - FBC, fasting glucose and lipids, prolactin, LH/FSH, TFTs, consider PSA, Testosterone
Validated questionnaire (IIEF or SHIM)
Specialised tests - penile doppler USS, nocturnal penile tumescence (rigiscan)
```
133
How to manage a patient with erectile dysfunction?
```
Lifestyle changes - stop smoking, weight loss, exercise, avoid alcohol excess
Optimise medication
Correct hormone imbalance
Counselling (if non-organic)
Vacuum device
```
134
How can PDE5 inhibitors be used to treat erectile dysfunction?
Sildenafil, Tadalafil, Vardenafil
Inhibits breakdown of cGMP by PDE5 leading to smooth muscle relaxation therefore prolonged erections
Not erectogenic
Side effects: headaches, flushing, nasal congestion, impaired colour vision, priapism
Success rate 80-85%
Failed (4 times at the highest dose)
135
Other than PDE5 inhibitors what are the treatment options for erectile dysfunction?
```
Intraurethral therapy - inserting the Alprostadil (prostaglandin E1) suppository into the penis to increase cAMP
Injectable therapy - intracavernosal injections o alprostadil (Caverjet). Side effects: pain, priapism, penile fibrosis.
Penile prosthesis (last line) - ineffective medical treatment, post treatment for priapism, transgender surgery.
Inflatable - 2 cylinders with a reservoir and a pump
Malleable - moved up and down
Risks: urethral perforation, cold glans, ‘concorde glans’, malfunction, infection, erosion
```
136
What is premature ejaculation?
Ejaculation which always/nearly occurs prior to within 1 min of vaginal penetration and the inability to delay and negative consequence of distress, frustration or avoidance of sexual intimacy’
Majority are psychological, occasionally found with endocrine disorders, parkinson’s disease and opioid withdrawal
137
How would you manage a patient with premature ejaculation?
Generally due to performance anxiety
| Treat with counselling, quiet vagina, squeeze technique, topical local anaesthetic, SSRIs
138
What is Peyronie’s disease?
Fibrotic plaque causing bend on erection
Cause unknown - associated with Dupytren’s contracture, alcohol excess, diabetes
Presents with pain on erection, deformity, inability to have penetrative intercourse.
Assessment with photos of erect penis in dorsal and lateral view to measure degree of bend
139
How would you treat Peyronie's disease?
Management is initially conservative
NES application (stitches on the other side of the bend)
Lues procedure - remove the plaque and put a graft in
Penile prosthesis
140
What happens in a penis fracture?
Uncommon
Excessive bending of penis while erect
Rupture of tunica albuginea
Classic history of sudden pain, immediate detumescence and inability to gain an erection
141
How to manage a patient with a penis fracture?
No role for conservative management
Theatre for exploration and repair
20% have ureteral injury
Delay in repair may lead to complete ED
142
What is Priapism?
Prolonged often painful, erection if penis in the absence of sexual desire or stimulation lasting more than 4 hours
Peak age 20-50 years
143
What are the causes of priapism?
Idiopathic (most common)
Haematological: sickle cell disease (most common cause in childhood), thalassaemia, fat emboli, Factor V leiden, G6PD deficiency
Neurogenic: SCI, CES, CVA
Infection: toxin mediated e.g. scopion sting, spider bite
Medications: vasoactive erectile agents, alpha blockers, antipsychotics, GnRH, antidepressants, spinal anaesthetic
Recreational drugs: alcohol, marijuana, cocaine
Metabolic disorders: gout, amyloidosis
Malignancy: locally advanced cancer or metastatic cancer, haematological malignancy
144
How would you assess priapism by taking a history?
```
Onset and duration of erection
Painful?
Previous episodes
Prior erectile function
Risk factors - sickle cell diseases prior trauma medication history, recreational drug use
```
145
How would you investigate Priapism?
FBP and U&E
Sickle cell screen
Cavernosal blood gas analysis
Examination after analgesia
146
How would you manage a patient with low-flow priapism?
Pain relief - penile block
Conservative measures - ice pack, ejaculation
Aspiration +/- irrigation until you get bright red blood
Intracavernosal phenylephrine (alpha agonist)
Surgical shunts
Penile prosthesis
147
Why do we use creatinine to measure kidney function?
Waste product of muscle metabolism
Purely excreted by the kidneys
Longstanding measure of kidney function
But not everyone’s muscle mass is the same, high muscle mass = increased creatinine
148
Why is ACR more accurate than creatinine?
We can measure albumin +/++/+++ concentration using a urine dipstick.
But albumin in urine can be diluted or concentrated depending on urine volume. Creatinine is excreted in the urine at a constant rate. Therefore the ratio of albumin to creatinine should be constant irrespective of urine volume.
149
How can the eGFR be used to stage kidney disease?
The ACR can be used to define and stage chronic kidney ratio.
GFR below 60 - chronic kidney disease
Below 15 doesn’t mean that your kidneys have completely failed.
150
What are the causes of chronic kidney disease?
```
Diabetes
Chronic glomerulonephritis
Cystic disease
Hypertension
Obstructive uropathy
Acute kidney injury
```
151
What are the risk factors for chronic kidney disease?
```
Diabetes
High blood pressure
Heart and blood vessel (cardiovascular) disease
Smoking
Obesity
Being African-American, Native American or Asian-American
Family history of kidney disease
Abnormal kidney structure
Older age
```
152
How to treat a reduced GFR?
Treat hypertension - ACE inhibitors, ARBs, B blockers, Calcium channel blockers, diuretics
Treat dyslipidemia
Treat CKD specific symptoms
Lifestyle changes (smoking, drinking, diet and exercise).
153
What are the treatment options for chronic kidney disease?
- Haemodialysis - 3 times a week for about 4 hours.
Can be done in hospital, in centre, at home.
- Peritoneal dialysis - a treatment that uses the peritoneum, and a cleaning solution called dialysate to clean your blood. Dialysate absorbs waste and fluid from your blood, using your peritoneum as a filter.
- Kidney transplant - dialysis performed beforehand, surgery easier to put at the front of the pelvis.
154
How sucessful are kidney transplants?
⅓ of kidneys don’t work when they are initially placed in the patient - sometimes take a while to ‘wake up’.
12% of patients get rejection in the first year
155
How is filtration measured in the kidney?
GFR (the amount of blood that the kidneys can filter in a given unit of time). Typically 120ml/min.
Measured as eGFR, estimated GFR by calculations based on serum creatinine.
Severity of kidney disease is reflected by eGFR
Below 45 you will experience complications (anaemia and bone disease symptoms)
156
What is used to calculate eGFR?
eGFR predicts creatinine generation from age, gender and race
Requires steady state
Extremes of muscle mass may be misleading (cachexia, body builders, amputees, liver disease).
157
What is Fanconi syndrome?
Rare
A syndrome of inadequate reabsorption in the proximal renal tubules of the kidney.
Result of the damage of the proximal tubule due to glycosuria, acidosis with failure of urine acidification, phosphate wasting, rickets/osteomalacia, aminoaciduria.
158
What is the effect of ACEi and ARBs in chronic kidney disease?
Indicated preferentially in proteinuric CKD only (glomerular hypertension)
A degree of eGFR reduction associated with their initiation is tolerated
But important to stop in the setting of acute insults (e.g. sepsis)
More risk of renovascular disease (upstream squeeze)
159
What is the action of renal potassium control?
K freely filtered and mostly reabsorbed in proximal tubule/loop of Henle
Distal secretion determine renal excretion
Governed by:
Distal delivery of Na
Aldosterone
Insulin and catecholamines drive cellular K uptake, buffering acute changes.
160
What is the action of Calcitriol?
Increases calcium and phosphate absorption from the gut
Suppresses parathyroid hormone
Deficiency causes secondary hyperparathyroidism
161
What is renal anaemia?
Anemia of renal disease is a hypoproliferative anemia resulting primarily from deficient erythropoietin (EPO) or a diminished response to it; it tends to be normocytic and normochromic. Treatment includes measures to correct the underlying disorder and supplementation with EPO and sometimes iron.
162
Where would you usually find presentation of Chlamydia and gonorrhoea?
Adult - Urethra, Endocervical canal, Rectum, Pharynx, Conjunctiva
Neonate: Conjunctiva
Atypical pneumonia also in neonatal Chlamydia
163
How do Chlamydia and Gonorrhoea present in males?
Dysuria and urethral discharge
Incubation time: 2-5 days (GC) 7-21 days (CT)
Asymptomatic: 10% (GC) 50% (CT)
Transmission female to male: 20-60/80% (GC) 70% (CT)
Complications occur mostly with CT: epididymo-orchitis; reactive arthritis
164
How do Chlamydia and Gonorrhoea present in females?
Non-specific symptoms – discharge, menstrual irregularity, dysuria
Incubation time: 50% (GC) 70% (CT)
Asymptomatic: 50% (GC) 70% (CT)
Transmission male to female: 50-90% (GC) 70% (CT)
165
What are the complications associated with Chlamydia and Gonorrhoea in females?
Pelvic inflammatory disease
Tubal factor infertility – damage to Fallopian tube
Increases risk of ectopic pregnancy
Scarring in the pelvis: chronic pelvic pain
Neonatal transmission
Ophthalmia neonatorum (conjunctivitis)
Atypical pneumonia with CT
Fitz Hugh Curtis syndrome – peri-hepatitis
166
How would you diagnose Chlamydia?
Difficult to culture so Nucleic Acid Amplification Tests (NAAT) e.g. PCR is used.
High specificity and sensitivity but negative test ≠ not infected.
Females: self-collected vaginal swab (more accurate)
Males: first void urine sample
167
Why is chlamydia screening in the community important?
Community based studies show prevalence of about 10% in asymptomatic <25 year olds
Asymptomatic carriage of Chlamydia for a number of years is well described
Community screening aims to reduce complications by reducing the prevalence of asymptomatic infection
168
What is the treatment for Chlamydia?
Partner management - screening
Test for other STIs including HIV
First-line treatment: Doxycycline 100mg bd for 7 days
Erythromycin 500mg bd for 14 days or Azithromycin in pregnancy
Antibiotic resistance not a clinically important problem
169
When would you use Azithromycin treatment for Chlamydia?
Azithromycin 1G as a single dose is the licensed dose
If Doxycycline isn't suitable
If there are concerns about co-infection with Mycoplasma genitalium
Used in pregnancy only if adequate alternatives not available.
170
How would you diagnose Gonorrhoea?
Microscopy of gram stained smears of genital secretions from male urethra, female endocervix or rectum looking for gram negative diplococci within cytoplasm of polymorphs.
Culture on selective medium to confirm diagnosis
Sensitivity testing – temperature and pH can affect the sample
NAAT (not time-sensitive)
171
What is the treatment for Gonorrhoea?
Partner notification!
Test for other STIs – syphilis and HIV
Continuous surveillance of antibiotic sensitivity
Single dose treatment preferred
Aim to cure at least 95% of people at first visit
Current regime – Ceftriaxone 1 gram IMI
172
Why is partner notification important in Chlamydia and Gonorrhoea diagnosis?
Prevent re-infection of index patient
Prevent complications in asymptomatic contacts
Protect unborn child
173
What is Syphilis?
Caused by Treponema pallidum subspecies pallidum
- Early infectious syphilis (within 2 years of infection)
Primary, Secondary and Early Latent
- Late syphilis (over 2 years since infection)
Late latent, CNS, CVS, gummatous
174
How is Syphilis usually spread?
Men who have sex with men through unprotected anal intercourse.
Oral sex.
175
What are the clinical features of primary syphilis?
Primary chancre - 95% genital skin, also nipples, mouth
Incubation ‘9-90 days’ - usually 21-35 days
Dusky macule - papule- indurated clean based non-tender ulcer. 50% solitary
Regional nodes 1-2 weeks after chancre
Untreated - heals without scarring in 4-8 weeks
176
What are the clinical features of secondary syphilis?
Onset 6-8 weeks after infection - primary chancre may be present concurrently (30%) or may have no history of primary chancre
70% present with skin rash – typically has an unusual distribution (trunk, arms, legs, on hands and face)
Other manifestations - mucous membrane lesions (30%), generalised lymphadenopathy (50-60%), alopecia (moth-eaten), hoarseness, bone pain, hepatitis, nephrotic syndrome, deafness, iritis, meningitis, cranial nerve palsies, constitutional
177
What are the complications of syphilis?
```
65% No clinical sequelae
15% Late benign gummatous (2 -40 years after)
10% Neurosyphilis (2-30 years)
Dementia
10% Cardiovascular (20-30 years)
Huge aortic aneurysm – heart failure
```
178
How is syphilis diagnosed?
Early moist lesions – may be able to identify motile spirochetes on wet mount using dark ground microscopy
Mainstay of diagnosis is serology
- Genital ulcer: Serology usually positive if ulcer present for 2 or more weeks. If serology negative, repeat at 6 and 12 weeks to exclude diagnosis
- Rash or other features of suspected secondary syphilis, serology can confidently confirm or refute the diagnosis
179
What are the serological tests for syphilis?
Enzyme immunoassay screening
Confirmatory tests for samples which screen positive: Treponema pallidum particle agglutination test (TPPA)
Non- treponemal test to assess disease activity
- Rapid plasma reagin (RPR), a syphilis blood test that looks for antibodies to the syphilis bacteria
- Rapid plasma reagin (RPR), a syphilis blood test that looks for antibodies to the syphilis bacteria
180
What is the treatment for syphilis?
Penicillin by injection is mainstay
| Efficient follow up and partner notification essential
181
What is the HIV/STI transmission model?
```
R = Rate at which organism reproduces itself – if >1 incidence will rise If <1 will decline
B = The chance of infection passing per potential exposure – depends on behavioural factors e.g. condom use/type of sex as well as microbiological characteristics of organism
C= Partner rate over time denotes number of opportunities for transmission – concurrent partnership patterns particularly effective at sustaining transmission
D = duration of infection reduced by easy access to services
```
182
What is sexual health?
Sexual health is a state of physical, emotional, mental and social wellbeing in relation to sexuality; it is not merely the absence of disease, dysfunction or infirmity.
183
What factors impact sexual health?
Individual factors - mental health, self-esteem, self-worth, self-image, dysfunction, spirituality, education, life experience, abuse
Social relationships - family, upbringing, peers, neighbours, colleagues, partnerships, marriages, children
Emotions - experience of different emotions, ability to cope, response to others
External and political factors - the law, media, religion, poverty, housing, refugee status, education, police
Social groups - class, gender, sexual orientation, race, ethnicity, disability, age, HIV status
Services - access to contraception, condoms, STI/HIV services, abortion, advice
184
How can STI transmission be prevented?
Primary Prevention: reducing risk of acquiring STI e.g STI awareness campaigns, one to one risk reduction discussion, vaccinations, Pre and post exposure prophylaxis
Secondary Prevention: case finding e.g. easy access to STI/HIV tests/treatment, partner notification, targeted screening
Tertiary Prevention: reducing morbidity/mortality e.g. Anti-retrovirals for HIV, Prophylactic antibiotics for PCP, Acyclovir for suppression of genital herpes
185
How to reduce the spread of HIV?
- Effective Condom Use
- Regular Testing
- Earlier access to Treatment
- Challenging stigmatising attitudes and assumptions
186
What is anti-retroviral primary prevention?
Post-exposure prophylaxis (PEP/ PEPSE)
Available A&E and Sexual health services
28 day course
Pre-exposure prophylaxis (PrEP)
PROUD study 2015: reduces HIV risk by 86% (positive clinical trials)
Treatment as Prevention (TasP) – retroviral treatment to prevent the spread of HIV
187
What is partner notification?
A public health activity that aims to control infection by identifying key individuals and sexual networks, warn the unsuspecting and attempt to break the chain of infection.
188
How are partners traced (STIs)?
- Patient Referral
- Provider Referral
- Conditional or Contract Referral
Emphasis on patient choice and confidentiality
189
What is a urinary tract infection?
Combination of clinical features and the presence of bacteria in the urine
190
What are the two types of UTI?
Lower tract: UTI, Cystitis
| Upper tract: Pyelonephritis (kidney)
191
How can UTIs be classified?
Asymptomatic bacteriuria
Uncomplicated
Complicated
192
What is bacteriuria?
The presence of bacteria in the urine
- Symptomatic
- Asymptomatic
193
What is pyuria?
Presence of leukocytes in the urine
Associated with infection
Sterile pyuria (finding white cells but can’t grow anything)
194
Who gets Asymptomatic bacteriuria?
Mostly in over 65s
Increased rates in hospital
100% in patients with catheters
195
Who gets complicated vs uncomplicated UTIs?
Uncomplicated - non pregnant women
Complicated - pregnant women, men, catheterised, children (more common in girls), recurrent/persistent infection, immunocompromised, noscomial infection, structural abnormality, urosepsis, associated urinary tract disease, renal transplant.
196
What are the most common pathogens that cause UTIs?
E. coli >50%
Proteus 10-15% (associated with renal stones)
Klebsiella 10% (hospital/catheter associated)
Enterococci 8-10% (low grade pathogen)
Staph.saprophyticus 5-8% (young women)
S.aureus 2-6% (may be indicative of a deep seated infection)
Pseudomonas aeruginosa 4% (Recurrent UTI/underlying pathology)
197
What increases the risk of a UTI?
```
Being a woman - urethra is shorter
Catheterisation allowing colonisation
Obstruction from prostatic hypertrophy
Bladder stones or tumour
Low urinary volume
Ureteric stones
Stasis during pregnancy
E.Coli fimbriae are adapted for bladder colonisation
Proteus spp produce urease which increases pH and stone formation
```
198
What are the symptoms of UTIs?
Lower UTI – dysuria, frequency
| Upper UTI – pyrexia, haematuria
199
How would you investigate a UTI?
Urine sample
Dipstick of urine
Culture
Sensitivities
200
What is tested for in urinalysis?
Nitrates and leucocytes to look at infection
Blood in upper tract infection or other things like infective endocarditis
pH is not the most reliable indicator but is also included
Glucose
Protein
Ketones
201
What are the different ways you can obtain a urine sample?
MSU – mid-stream urine to get a representative sample of urine
CSU – catheter urine
Clean catch in paediatric
SPA – suprapubic aspirate
Early morning urine – when looking for TB
Bag urine
202
What would you look for in microscopy testing in urine?
White blood cells - > 10^4 wbc/ml (pyuria)
Red blood cells
Casts - give clues to renal pathology and can be indicative of infection, may show damage to kidney epithelium (glomerulonephritis)
Bacteria - Counts >10^5 cfu/ml Indicative of infection
10^4-10^5: Doubtful significance. <10^4: Contaminant
Epithelial cells - May indicate a poorly taken specimen (shedding from the perineum)
203
How would you culture a urine sample?
CLED plate at 37 degrees
24-48 hours
Chromogenic agar can give different colours for different microorganisms
Sterile pyuria – symptoms but cannot grow anything in the lab. This might be due to TB, mycoplasma, candida.
204
How to manage UTIs?
If >65 with asymptomatic bacteruria then do not treat
Uncomplicated - MSU not necessary, but if it is adjust antibiotics accordingly. 3 days Nitrofurantoin.
Adjunctive advice: increase fluid intake, void pre – post intercourse and information about hygiene.
Complicated - Any UTI in the presence of a structurally or functionally abnormal urinary tract, with or without host compromise. Always send a sample.
Antibiotics for 7 days.
205
What is the first line antibiotic treatment for UTIs?
Avoid broad spectrum antibiotics
Nitrofurantoin
Avoid in pregnancy
Avoid if renal function Cr Cl< 45 ml/min
Side effects
206
What are some new antibiotics that can be used for treatment of UTIs?
Oral agents
Fosfomycin
Pivmecillinam
207
What should you be aware of when taking catheter samples of urine?
All become colonised (7-32 days)
Cultures should always be sent (fresh sample, not from bag) – interpret with caution
Do not dipstick
Change or remove catheter when starting treatment
208
How do catheters cause UTIs?
Insertion may carry organisms into the bladder
At risk of infection up to 24 hours post removal
Hospitable environment in the catheter
Formation of biofilms (protected from flow of urine, host defences and antibiotics)
Incomplete voiding
209
What are the risks of short and long term catheters?
Short term catheters: only in for a couple of days, at risk of monomicrobial infections
Long term catheters: at risk of polymicrobial infections and complications: UTI/Pyelonephritis, Stones, Obstruction, Chronic inflammation
210
How to prevent CA-UTI?
```
Prevention of catheterisation
- Intermittent catheterisation
- Suprapubic catheterisation
Prevention of bacteriuria
- Keep catheter closed
- Remove as soon as possible
Prevention of complications
- Don’t treat if asymptomatic
- Catheter replacement
```
211
What increases the risk of UTI in pregnancy?
```
Age
Parity (number of times that she has given birth to a fetus with a gestational age of 24 weeks or more)
Sexual activity
Diabetes
Previous UTI
```
212
How should UTIs in pregnancy be investigated and treated?
Culture rather than dipstick
Positive cultures should be confirmed with a second sample
Asymptomatic bacteriuria should be treated (unlike elderly) -20-40% untreated bacteriuria develop acute symptomatic pyelonephritis
Test of cure should be sent 1 week after treatment
213
What is Pyelonephritis?
Infection of the renal parenchyma and soft tissues of renal pelvis /upper ureter
Predominantly affects women <35
Associated with significant sepsis and systemic upset, rigors
Often fluid depleted –require prompt resuscitation
214
What are the symptoms of Pyelonephritis?
Classical triad
- Loin pain
- Fever
- Pyuria
215
What are the routes of infection for Pyelonephritis?
Ascending: Urethra colonised with bacteria. Massage of the urethra during intercourse can force bacteria into the female bladder
Haematogenous: S.aureus/Candida
Lymphatic spread: Rare
216
How would you investigate Pyelonephritis?
Abdominal examination - tender loin, renal angle tenderness, vaginal exam to rule out tubal/ovarian/appendix pathology
Bloods including cultures
U/S scan - to rule out obstruction in upper tract
Mid-stream urine
217
How would you treat Pyelonephritis?
Fluid replacement – increased losses
IV Abx – Broad spectrum eg. Co-amoxiclav +/- Gentamicin
Drain obstructed kidney
Catheter
Analgesia
Complete 7-14 days (depending on choice of antibiotic)
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What are the complications of Pyelonephritis?
Renal abscess - Slow/no response to antibiotics, imaging, more common in diabetics
Emphysematous pyelonephritis - rare, gas accumulation in the tissues, life threatening, may need nephrectomy
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How common are urinary stones?
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Increasing incidence: 10-15% lifetime risk
Unusual in children
1 in 12 women
1 in 6 men
Commonest age 30-50 but decreasing
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Where can you get stones in the urinary tract?
Anywhere from Collecting duct to External Urethral Meatus
Upper urinary tract: ureters and kidneys
Lower urinary tract: bladder, prostate, urethral
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Why do patients get urinary stones?
Anatomical factors
- Congenital (horseshoe, duplex, PUJO, spina bifida)
- Acquired (obstruction, trauma, reflux)
Urinary factors
- Metastable urine, promoters and inhibitors
- Calcium, Oxalate, Urate, Cystine
- Dehydration
Infection (less common due to antibiotics)
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How are urinary stones made?
“Nucleation theory” suggest that stones form from crystals in supersaturated urine
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What are urinary stones made of?
Most are formed of crystals of normal urinary constituents
80% Ca2+ based – oxalate, phosphate
10% uric acid – usually lucent on KUB XR
5-10% struvite – infection stones
1% cystine – congenital (“COLA” - cysteine, ornithine, lysine, and arginine)
Rarities – Drug stones, including indinavir, ephedrine
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How can urinary stones be prevented?
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Overhydration – 2.5-3L/24hr Urine output
Low salt (sodium) diet
Normal dairy intake
Healthy protein intake (<50-100g/day)
Reduce BMI (metabolic syndrome)
Active lifestyle
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How can uric acid stones be prevented?
Since uric acid stones only form in acidic deacidification of urine to pH7-7.5 is preventative.
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How can cysteine stones be prevented?
Excessive overhydration
Urine alkalinisation
Cysteine binders (eg Captopril, Penicillamine)
+/- genetic counselling
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What symptoms can urinary stones cause?
Asymptomatic
Loin to groin pain
“Renal” colic
UTI symptoms: dysuria, strangury (bladder ‘tied in knots’, urgency, frequency
Recurrent UTIs
Haematuria: visible and non-visible (85%)
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What is renal colic?
Pain results from upper urinary tract obstruction
Unilateral loin pain
Rapid onset
Unable to get comfortable – writhing
Radiates to groin and ipsilateral testis/labia
Associated nausea/vomiting
Spasmodic/colicky, worse with fluid loading
Classically severe
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How would you investigate urinary colic?
Airways, breathing, circulation and give analgesia/antiemetic
Focused history and examination
Urinalysis, Midstream urine (MSU) if +ve
FBC, U+E, Calcium, Uric acid
Imaging:
- Non-contrast computerized tomography (NCCT-KUB)
- Kidney, ureter, bladder X-ray (KUBXR)
- Ultrasound scan
- Intravenous urogram (IVU): rarely used, but almost as good as NCCT for acute ureteric colic
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What are the potential differential diagnoses for urinary colic?
Vascular accident – ruptured AAA (>50yo) until proven otherwise
Bowel pathology – diverticulitis, appendicitis
Gynae – ectopic pregnancy, ovarian (cyst) torsion, testicular torsion
Musculoskeletal
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How is KUBXR useful for urinary colic?
Historical first line investigation but not used as much nowadays
Only 50-60% sensitive in comparison to CT
If stone visible then greatly aids follow up
May avoid repeated CTs
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How is NCCT-KUB useful for urinary colic?
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Non-contrast Computerised Tomography – Kidneys, Ureter, Bladder
Very rapid (one breath hold)
99+% sensitive for stones Specificity ~90%
No contrast (allergies, renal function)
Other pathology/organs
But:
No functional info
Carries a fairly high radiation dose
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What should you look for on a NCCT-KUB?
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Number of kidneys
Condition of kidneys:
- Perinephric tissues
- Cortical thickness
- Hydronephrosis +/- hydroureter (swelling)
- Any visible stones
Consider any other pathology
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How is ultrasound scan useful for urinary colic?
Sensitive for hydronephrosis (not all acute obstructions dilate)
Very poor at visualising stones in ureter
Useful in pregnant and younger recurrent stone-formers (no radiation risk)
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How would you manage urinary colic?
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Analgesia
NSAID suppository
Opiates
Antiemetic/s
+/- Admit
+/- IV fluids
May make pain worse as diuresis ensues
Observe for SEPSIS
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Why is it important to consider infection in cases of urinary colic?
Pyonephrosis: combination of infection and obstruction
Can lose renal function in 24 hrs
Can lead to systemic sepsis leading to septic shock
IV Antibiotics, Oxygen, drainage of kidney by Nephrostomy or Ureteric stent
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What are the treatment options for urinary stones?
Depend largely on site and size of stone, patient factors and complications / risks
Conservative
Medical
Lithotripsy (externally break stones up)
Surgical
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Are kidney stones dangerous?
Smaller ones can migrate into ureter
Larger stones occlude calyces and/or pelvic ureteric junction
Can acutely obstruct – renal or ureteric colic
Chronic renal damage (esp. if infection stone)
- abscess
- fistulae
- XPN (xanthogranulomatous pyelonephritis)
BUT small stones (<1cm) can be observed, and only 1/3 will progress
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How to treat renal stones?
Conservative – small, safe location, asymptomatic, static size, comorbid++
Extracorporeal shock wave lithotripsy – up to 1-2 cm, problems with fragment passage and clearance
Ureteroscopic – flexible, laser only,<2 cm
Percutaneous nephrolithotomy –ideal for larger stones
Nephrectomy – if split function <10-15%
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How to treat ureteric stones?
Conservative – allow 2 weeks to pass
Majority <4mm will pass, only ~10% >7mm
Drainage if sepsis
Medical expulsive therapy – awaiting supporting evidence
Extracorporeal shock wave lithotripsy – stones <1cm
Ureteroscopy – suitable for any stone, laser, basket extraction, lithoclast
Laparoscopy/open surgery (rare)
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How to treat bladder stones?
Conservative - asymptomatic/unfit
Endoscopic - can be accompanied by treatment of bladder outlet obstruction
Open / Laparoscopic surgery - ideal for larger stones or if other open procedures required
