Phase 2 - Renal & GU Flashcards
What is Nephro/Urolithiasis
A solid crystellisation of minerals found in the urine - can be:
- KIDNEY (from renal pelvis) stones
- URETRIC stones
Can get stuck within kidney, ureter, bladder or urethra.
10-15% lifetime risk. More common in MALES 30-50 y/o.
Pathophys of Nephrolithiasis + types of stones
Solute conc exceed saturation (esp in collecting duct?)
-> SUPERSATURATED URINE
- FAVOURS CRYSTALISATION (oft triggered by something)
Can cause OUTFLOW OBSTRUCTION (within renal parencyma or collecting system -> urinary tract) -> HYDRONEPHROSIS (complication)
Formed by deposit of:
- CALCIUM OXALATE (radiopaque - 80-90%)
- URIC ACID/urate (RADIOLUCENT - much less common - 10%)
- CALCIUM PHOSPHATE
- STRUVITE (phosphate - 5-10% linked to INFECTIONS esp PROTEUS)
- Cystine (derivative of cysteine - uncommon)
What occurs in Hydronephrosis
DILATION + OBSTRUCTION of RENAL PELVIS
- INCREASED DAMAGE + INFECTION risk
(esp as obs causes prostaglandin release which can increase glomerular filtration)
Management of Hydronephrosis
Requires SURGICAL DECOMPRESSION ASAP
Where are renal/uretric stones most likely to be found
- Uretropelvic/Pelviuretric junction (RENAL PELVIS MEETS URETER)
- PELVIC BRIM
- VESICOURETRAL junction (URETER MEETS BLADDER)
Risk factors/causes for renal stones
- ANATOMICAL:
- Congenital horseshoe kidney
- spina bifida
- Obstruction to urinary tract
- TRAUMA
- CHEMICAL COMPOSITION of urine that favours stone crystalisation
- High calcium, urate, oxalate, struvite or cysteine
- CHRONIC DEHYDRATION (esp for uric acid stones)
- PRIMARY KIDNEY DISEASES (e.g. PKD/renal tubular acidosis)
- UTIs (many hydrolyse urea -> ammonium hydroxide)
- can form large mixed stones of Magnesium, Ammonium phosphate + Calcium
- increased ammonium + alkalinity favour stone formation
- can form large mixed stones of Magnesium, Ammonium phosphate + Calcium
- DRUGS e.g. diuretics, antacids, acetazolamide, corticosteroids, aspirin, allopurinol, vitamin C/D
- Hx/Family Hx of renal stones
- Obesity (lowers pH)
More specific, focus on above if struggling
- Uric acid stone RFx
- GOUT (for uric acid stones) or HYPERURICAEMIA
- Ileostomy patients -> dehydration + bicarb loss via GI secretion -> acidic urine (uric acid LESS soluble in acid -> stones)
- HIGH SALT/OXALATE intake (chocolate, tea, rhubarb) -> HYPEROXALURIA
- Low Ca2+ intake can -> decreased binding of oxalate to Ca2+ -> increased oxalate absorption urinary excertion
- GI disease e.g. Crohn’s -> increased oxalate GI resorption
- HYPERPARATHYROID (hypercalcaemia +/- hypercalciuria)
- Cystinuria - autosomal recessive - affects cystein in renal tubule/GI epithelial cells -> excessive urinary excretion/formation of cysteine stones
Slightly more common in MALES; 20-40 y/o (uncommon in children)
Symptoms of renal stones
Can be asymp
- ACUTE LOIN TO GROIN (/ipsilateral testis/labia) PAIN (Renal colic)
- Rapid onset (can be woken from sleep)
- COLICKY (in WAVES from ureteric peristalsis)
- FLUID/DIURETICS make pain WORSE
- CAN’T LIE STILL (diff from peritonitis/biliary)
- N + V
- Haematuria + dysuria (may get pyuria or other UTI symps)
- Recurrent UTIs - esp if voiding impaired
- RED FLAG - FEVER (superimposed infection e.g. pyelonephritis)
Bowel sounds may be reduced; BP may be low
Diagnosis of renal stones + Diff diagnoses
If over 50, assume vascular accident (e.g. AAA) until otherwise proven
- PAIN HISTORY
- URINALYSIS/dipstick - haematuria, pregnancy (esp ECTOPIC), ovarian cyst (might have torsion) etc. + check for RBCs, protein/glucose
- Midstream urine MC+S - for UTI
- BLOODS:
- FBC
- U+E - if DERANGED - suggests HYDRONEPHROSIS
- creatinine
- Calcium and Uric acid
- 1st LINE: Kidney, Ureter, Bladder (KUB) XR
- (80% specific, cheap, easy)
- GOLD: NON-CONTRAST CT KUB - DIAGNOSTIC
- (rapid; no functional info + each scan -> ~18mth background radiation)
US rarely used acutely (poor visualisation) - helpful in pregnant/younger RECURRENT patients
+ sensitive for hydronephrosis
Diff diagnoses:
- AAA
- Diverticulitis, appendicitis
- Ectopic pregnancy (pregnancy test)
- Testicular torsion
Complications of stones + Why should you never use contrast for suspected kidney issues
Complications:
- Pyonephrosis (suppurative (pus producing) upper tract infection),
- fistulae,
- CKD,
- Xanthogranulomatous pyelonephritis (chronic infection of kidneys caused by stones)
Contrast needs to be excreted by kidney but is composed of HEAVY metals (large molecules)
-> HARMFUL if kidney unable to excrete properly
Treatment of renal stones
- Symptomatic:
- IV FLUIDS/HYDRATE
- ANALGESIA (NON-OPIATE)
- NSAID e.g. IV DICLOFENAC for severe pain
- antiemetics if needed
- observe for SEPSIS
- Nephrostomy if required (tubes inserted in the back and enter kidney pelvis, draining urine)
- Ureteric stent – tubes inserted up ureters and bypass stones if necessary
- Antibiotics if UTI (e.g. IV CEFUROXIME/GENTAMICIN)
- prevent pyonephrotic renal failure/sepsis
- If <5mm:
- oft pass spontaneously - WATCH + WAIT
If too big/causing pain:
- Medical expulsive therapy:
- ORAL NIFEDIPINE or alpha blocker e.g. ORAL TAMSULOSIN can promote expulsion and reduce analgesia
- Surgical elective
- EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL)
- 6-10mm (max 20mm)
- URETHROSCOPIC LASER REMOVAL or BASKET EXTRACTION
- PERCUTANEOUS NEPHROLITHECTOMY (PCNL)
- > 20mm/multiple/complex
- Consider uretroscopy with YAG laser
- NEPHRECTOMY if severe
- Laproscopic/open surgery for bladder stones
- EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL)
Why do you not give opiates for kidney problems
Opiates renally excreted
- if kidney excretion impaired - opiates stay in body
-> HARMFUL, can overdose
Where can causes of AKI/CKD originate from AKA classes of AKI/CKD
- Pre-renal
- Intrinsic
- Post renal
Pre-renal causes of AKI
Hypoperfusion
-
HYPOVOLEMIA/REDUCED Cardia Output
- congestive HF
- Shock/sepsis
- Diarrhoea/vom
- RENAL ARTERY STENOSIS
- Some DRUGS - REDUCE BP, circ volume or GFR:
- Liver failure
Intrinsic/Renal causes of AKI
- Tubular:
- ACUTE TUBULAR NECROSIS (ATN) - main (linked iscahemia + some nephrotoxic e.g. Nsaids, contrast, antibiotics)
- MYELOMA
- RHABDOMYOLYSIS
- lymphoma infiltration
-
Intersitial:
- Acute interstitial nephritis (typically presents days-week after drug admin -> oliguria, fever (50%), eosinophilia + sometimes rash) - i.e. allergic reaction
- lymphocytic infiltration (hypersensitivity reaction to infection)
- VASCULAR
- (vasculitis, thrombosis, embolism, dissection)
- Glomerular
- GLOMERULONEPHRITIS
- Toxins + nephrotoxic drugs
- NSAIDs
- ACE-I (constricts afferent arteriole)
- ARBs
- loop diuretics
- IV contrast
- TUMOUR LYSIS syndrome
Post-renal causes of AKI
Obstructive
- STONES
- BENIGN PROSTATIC HYPERPLASIA
- External COMPRESSION of URETER (tumours etc)
- OCCLUDED indwelling CATHETER
- NEUROGENIC BLADDER
- Some drugs like anticholinergics + CCBs
Define AKI
Abrupt decline in kidney function (hrs - days) - covers a spectrum of injury/causes (it’s a syndrome rather than biochemical diagnosis)
- Characterised by:
- INCREASED SERUM CREATININE/urea
- DECREASED URINE OUTPUT
NICE Diagnostic criteria (KDIGO classification) for AKI
Any 1 of below:
- INCREASED CREATININE by >= 26 µmol/L in 48 hours
- > = 50% INCREASED CREATININE over 7 DAYS
- REDUCED URINE OUTPUT:
- < 0.5 ml/kg/hour for > 6HR (adults)
- < 0.5 ml/kg/hour for > 8HR (kids)
- normal = 0.5-1.5 ml/kg/hr
Risk factors for AKI
- CKD
- OLDER age (>65)
- COMORBIDITIES
- DIABETES
- LIVER DISEASE
- HEART FAILURE
- HYPOVOLAEMIA
- NEPHROTOXIC DRUGS
- NSAIDs + ACE-I
- anticholinergics
- CCBs
- Optiates
- CONTRAST
- Cognitive impairment
Pathophys of AKI + its complications
Decreased filtration/urine output
-> ACCUMULATION of usually excreted substances
- K+: HYPERKALAEMIA
- Arrhythmias
- Urea: HYPERURAEMIA
- Pruritis from skin deposits + Uremic frost
- CONFUSION if severe
- (urea -> ammonia -> encephalopathy)
- Fluid: OEDEMA
- H+: ACIDOSIS
Top 3 causes of AKI
- SEPSIS
- CARDIOGENIC SHOCK
- MAJOR SURGERY
Signs/symptoms of AKI
Remember - all due to SUBSTANCE ACCUMULATION:
- ARRHYTHMIAS (K+ accumulation)
- METABOLIC ACIDOSIS (H+ retention)
- URAEMIA:
- ENCEPHALOPTHY
- Pericarditis
- Skin manifestations (e.g. pruritis)
- FLUID OVERLOAD: - or HYPOVOLEMIC SHOCK (pre-renal)
- OEDEMA
- OLIGURIA (<400 ml/day)/anuria
- potentially palpable bladder
Diagnosis of AKI
- 1ST LINE: UREA + ELECTROLYTES
- K+, H+, urea
- ESTABLISH CAUSE:
- UREA:CREATININE (urine dipstick)
- > 100 = PRE-RENAL
- < 40 = RENAL
- 40-100 = POST-RENAL
- UREA:CREATININE (urine dipstick)
- FBC + CRP (infection)
- VERY HIGH OR LOW WCC -> SUGGESTS SEPSIS
- RENAL BIOPSY (DIAGNOSTIC for INTRARENAL)
- USS (DIAGNOSTIC for POST-RENAL)
Other tests:
- ECG -> HYPERKALAEMIA
- Absent P wave, prolonged PR interval, Tall tented T waves, wide QRS complexes
- urine dipstick
- CXR
- ABG
AKI management
- Treat complications:
- CALCIUM GLUCONATE - hyperkalaemia
- or Insulin with Glucose (milder - insulin shifts potassium into cells but need glucose to stop hypo)
- SODIUM BICARB - acidosis
- DIURETICS - fluid overload
- CALCIUM GLUCONATE - hyperkalaemia
- STOP nephrotoxic DRUGS
Treat underlying cause
- LAST RESORT - RENA: REPLACEMENT THERAPY
- Haemo DIALYSIS - Indicated in:
- Acidosis
- Fluid overload
- Uremia (symptomatic)
- K+ >6.5/ ECG change
- (think AFUK)
- Haemo DIALYSIS - Indicated in:
Common Nephrotoxic drugs
- NSAIDS
- Aminoglycides
- ACE-i
- ARB
- Loop diuretics
- ?Metformin
- ?Digoxin
- ?Lithium - Any heavy metals can cause damage, esp if kidney is already struggling
Classification of AKI stages
- 1:
- CREATININE 1.5-1.9x Baseline or
- Urine REDUCED <0.5 ml/kg/hour for >= 6HR
- 2:
- CREATININE 2.0-2.9x Baseline or
- Urine REDUCED <0.5 ml/kg/hour for >= 12HR
- 3:
- CREATININE >= 3.0x Baseline or
- Urine REDUCED <0.5 ml/kg/hour for >= 24HR
Define CKD
Abnormal kidney structure/function
- eGFR <60mL/min/1.73m^2 for >3 MONTHS
- OR eGFR <90 ml/min/1.73m2 + signs of renal damage
- or Albumin:Creatinine >3mg/mmol
(normal = 120)
Classification of CKD stages
Based on GFR range:
- 1: >90 ml/min (w/ signs of renal damage)
- 2: 60-90 ml/min (w/ signs of renal damage)
- 3a: 45-59 ml/min
- 3b: 30-44 ml/min
- 4: 25-29 (severe)
- 5: <15 (Kidney FAILURE)
Causes/risk factors of CKD
Main:
- DIABETES M
- HTN
Also:
- glomerulonephritis
- PKD
- nephrotoxic drugs (esp NSAIDs)
Pathophys of CKD
Many nephrons damaged
- REDUCED GFR + INCREASED BURDEN on other nephrons
- COMPENSATORY RAAS to RAISE GFR
- INCREASED TRANSGLOMERULAR PRESSURE
- SHEARING
- LOSS OF SELECTIVE PERMEABILITY (protein/haematuria)
- INCREASED TRANSGLOMERULAR PRESSURE
- ANGIOTENSIN 2 upregulates TGF-beta + Plasminogen activator inhibitor 1
- Causes MESANGIAL SCARRING
Symps due to substance accumulation + diabetic nephropathy
Complications of CKD
- ANAEMIA (reduced EPO)
-> Pericarditis + effusion if severe - OSTEODYSTROPHY (reduced vit D activation)
- NEUROPATHY/ ENCEPHELOPATHY
- HTN, ^lipids, vasc calcific -> CVD (highest mortality)
Diagnosis of CKD
- FBC (anaemia of chronic disease)
- U + E (high urea + creatinine)
- raised PTH if stage 3 or more
- raised alk phos from bone dystrophy
- US (bilateral renal shrinking - can be large if infiltrative e.g. amyloidosis)
- GFR FUNCTION STAGING
- low eGFR
- URINE DIP (PROTEINURIA)
- Albumin-Creatinine RATIO >3 = SIG. PROTEINURIA
Management of CKD
NO CURE, it’s irreversible - treat complications
- lifestyle changes
- Anaemia: EPO + IRON (give iron first)
- Osteodystrophy: Vit D supplements
- Oedema: diuretics
- CVD: ACE-I + STATINS
- ATORVASTATIN
If END-STAGE (stage 5):
- RRT (dialysis)
- RENAL TRANSPLANT (cure)
Types of RRT
Non-continuous:
- Haemodialysis (short + max solute clearance but haemodynamic instability)
- Peritoneal dialysis (slower, less efficient, risk of peritonitis or abdo compartment syndrome but doesn’t require vascular access)
Continuous - used in ICU:
- Haemodiafiltration
- Haemofiltration
Continuous allows you to add in fluid and better control their fluid volume - needs to be continuously attached to machine
How is RRT typically administered (excluding peritoneal)
Vascular access
- AV Fistula (makes vein larger at connection)
- AV Graft (artificial plastic tubing that acts as vein if actual vein too small)
- Central venous catheter (temporary plastic tube inserted in large vein, typically in neck but could be in groin - usually only for emergancy haemodialysis)
AKI vs CKD
- Definition:
- AKI defined as RAISED SERUM CREATININE + Reduced urine output
- CKD = reduced eGFR
- Symptom onset:
- AKI = shorter onset
- CKD = 3+ months
- Anaemia:
- AKI = NO ANAEMIA
- CKD - ANAEMIA OF CHRONIC DISEASE
- US:
- AKI = NORMAL US
- CKD = BILATERAL SMALL ATROPHIED KIDNEYS
Types of incontinence
- Stress incontinence
- related to sphincter weakness
- leaks when INTRA-ABDO pressure RISE
- (more common in FEMALES)
- Urge incontinence
- Related to overactive bladder
- Mixed
- Overflow incontinence (retention -> leaking)
Basic Neuro-urology
- Cortex
- Sensation
- Voluntary initiation
-
PONTINE MICTURITION CENTRE/Peri Aquaductal Grey
- Co-ordination
- Completion of voiding
- Spinal Reflexes (S 2-4 - parasymp nerves S3, 4, 5 -> detrusor contraction + sphincter relaxation)
- Reflex bladder contraction
- Sacral micturition centre
- Guarding reflex
- Onuf’s nucleus
- Receptive relaxation
- Sympathetic (T10 - L2)
- Inhibits detrusor contraction + smooth muscle sphincter contraction
- Sympathetic (T10 - L2)
- Reflex bladder contraction
- External urethral sphincter (striated sphincter)
- Somatic (skeletal muscle) - overrides autonomic till appropriate to void
Classification of Lower Urinary Tract Symptoms (LUTS)
- Storage
- Voiding
- Post-micturition
Important to learn diff types in each category esp storage + voiding symptoms
Storage related LUTS
- FREQUENCY
- URGENCY (when they need to go, can’t hold it long - very desperate)
- NOCTURIA - esp in older men (prostate prevents full emptying -> leftover creates need to go at night when everything is relaxed)
- INCONTINENCE
Voiding related LUTS
- SLOW stream/Poor flow
- HESITANCY
- STRAINING (using abdo muscles)
- Intermittency
- TERMINAL DRIBBLE
(- Splitting/spraying)
(- Vesicle tenesmus (incomplete bladder emptying))
Post-micturition related LUTS
- Post-micturition dribble (later than terminal dribble)
- Feeling of INCOMPLETE VOIDING (contributes to frequency)
Definition of Over Active Bladder
URGENCY WITH FREQUENCY, with or without nocturia, when appearing in ABSENCE of LOCAL PATHOLOGY
Can be wet or dry
How is detrusor overactivity defined
A rise in PRESSURE on FILLING on URODYNAMIC TESTING
Briefly, how does urodynamic testing work
- Bladder is filled with fluid
- Pressure in bladder is measured
- Pressure in abdo is also measured (via rectum)
- Subtract pressure measured in bladder from intra-abdominal pressure for actual bladder pressure
Reserved for cases where surgery is considered/bladder safety is potentially compromised
Causes of Stress incontinence
- NEUROGENIC
- Congenital
- IATROGENIC (e.g. after prostectomy, leaving catheter in too long)
- In FEMALES, oft related to BIRTH TRAUMA:
- denervation of pelvic floor/urethral sphincter
- weakening of fascial support
- oft related to straining e.g. lifting weights
Treatment of Stress incontinence (+ main contraindication)
- Men:
- ARTIFICIAL SPHINCTER
- Women:
- Autologous sling
- Artificial sphincter
CANNOT DO if RISK of UNSAFE bladder (i.e if they have loss of compliance and you add a functional sphincter -> unsafe)
Management of urge incontinence
- Behavioural therapy
- Bladder diary
- reduce caffine/alcohol
- ANTI-MUSCARINICS
- BLOCK M2/M3 receptors (parasymp)
- S/E = dry mouth
- B3 AGONIST - MIRABEGRON
- increase SYMPATHETIC activity
- Botox
- muscular PARALYSIS (blocks ACh at neuromuscular junction)
- INCOMPLETE BLADDER EMPTHYING -> catheterise 15%
- SACRAL NEUROMODULATION (expensive)
- neg feedback
- shouldn’t work in complete spinal injury
- Surgery
- Augmentation CYSTOPLASTY
- may cause retention
Briefly, what happens in a cystoplasty
- Cut bladder in half (stop contraction)
- Put section of bowel in bladder
3 categories of neurogenic bladder conditions
- Suprapontine (cerebral)
- Voiding is CO-ORDINATED but SOCIALLY INAPPROPRIATE
- Suprasacral spinal cord conditions (SPASTIC)
- upper motor neurone damage
- Detrusor-sphincter dyssynergia (loss of co-ord)
- Potentially UNSAFE
- Sacral spinal cord conditions (FLACCID - conus damaged)
- loss of guarding and potentially compliance
Spastic vs Flaccid
Spastic - upper motor neurone lesion
- hyper-reflexia
- increased tone
- No sensation
- In bladder - spinal cord telling to squeeze but striated sphincter not relaxed
- UNSAFE
Flaccid - lower motor neuron lesion
- Hyporeflexia
- Reduced tone
- No sensation
- In bladder - no spinal cord control -> fills up, continuous leaking
What is an unsafe bladder
Bladder that can cause damage to kidneys via PROLONGED HIGH PRESSURES
What causes voiding problems
Usually in MALES
- OBSTRUCTION
- stones
- BENIGN PROSTATE HYPERPLASIA/enlargement
- Abdo masses/prolapse (vaginal/rectal)
- Urethral stricture (trauma or infection)
- FLACCID PARALYSIS/Atonic bladder - detrusor underactivity
Treatment of voiding LUTS
- ALPHA BLOCKERS +/- 5 alpha reductase inhib for BPH
- alpha blockers relax muscles around urethra
- 5 alpha-reductase inhibitors reduce levels of DiHydroTestosterone (DHT). Prostate shrinks when less DHT present.
- Prostatectomy
- LONG TERM CATHETERISATION
- potentially sacral neuromodulation
Normal role/anatomy prostate and the role of DHT
Prostate secretes fluid into urethra that nourishes/protects sperm.
Normal prostate is around walnut sized, has a midline indent, is symmetrical and the consistancy of the tip of your nose
- It produces prostate-specific antigen (PSA) - liqifaction of semen. Raised in serum if cancerous, hyperplastic, inflamed, infected (sexual activity).
DHT is the most potent androgen and one that cannot convert to oestrogen.
- 5 ALPHA-REDUCTASE converts TESTOSTERONE to DHT in PERIPHERAL TARGET TISSUES (paracrine - only has effect in vincinity of gland secreting it/where it is synthesised).
- Mainly in liver
- Stimulates sexual differentiation of organs in embryo
- Promotes PROSTATE GROWTH, sebaceous gland activity, male pattern baldness and body hair after puberty
Define benign prostatic hyperplasia
Non-malignant prostate hyperplasia (increase in number of epithelial/stromal cells - look up in histology book)
- normal w/ aging
Risk factors for BPH
- increased AGE
- ethnicity (Afro-Caribbean = increased testosterone)
CASTRATION is PROTECTIVE
Pathophys of BPH
Proliferation of epithelial/stromal cells in INNER TRANSITIONAL ZONE of prostate
- causes narrowing of urethra
Presentation of BPH
- LUTS esp VOIDING RELATED
- Voiding:
- Poor stream; Dribbling
- Vesicle tenesmus/incomplete emptying
- Straining
- Potential dysuria (painful urination)
- Storing:
- Frequency, urgency, Nocturia (>30%),
- Incontinence
- Voiding:
If totally occluded - may get ANURIA
-> RETENTION, HYDRONEPHROSIS, UTI, stones
Investigation of BPH
DRE (digital rectal exam)/PR (per rectal) exam
- Prostate feels SMOOTH and ENLARGED, may have very defined or obliterated midline sulcus depending on size (normal prostate is around walnut sized, has a midline sulcus (usually not very defined), is symmetrical and the consistancy of the tip of your nose)
PSA to try and rule out cancer (more commonly raised in cancer) but PSA can be raised in both
Also exclude things like stones and UTIs
Treatment for BPH
- LIFESTYLE: reduce CAFFINE (it’s a diuretic - this is just to reduce urgency/frequency)
- May ACUTELY need catheter
- Drugs:
- 1ST LINE: ALPHA BLOCKER - TAMSULOSIN (relaxes bladder neck)
- 2ND LINE: 5 APLHA REDUCATSE INHIB - FINASTERIDE (reduces DHT -> reduces prostate size)
- Lowers PSA so may hide cancer + risk of sexual dysfunction
- Surgery last resort
- TURP - TransUrethral Resection of Prostate
- COMPLICATION - retrograde ejaculation
- TURP - TransUrethral Resection of Prostate
Define/pathophys of prostate cancer
Neoplastic, malignant proliferation of outer PERIPHERAL zone of prostate. Can also affect transitional zone in 20%. (central zone seems pretty resistant to pathologies)
- main cause of male malignancy
It is usually an ADENOCARCINOMA (glandular epithelium)
Spread may be:
* Local → Locally advanced: seminal vesicles, bladder and rectum
* Via lymph
* Haematogenously - bone (sclerotic bony lesions) or less common; brain, liver and lung
Androgen receptors on the prostate are responsible for cancerous growth
- can get castration-resistant cancer which is still androgen sensitive
Risk factors for prostatic cancer
- Genetic: mutations in BRCA2, HOXB13 (linked to <55 y/o cancer)
- FHx
- 3 or more affected relatives or
- 2 relatives who have developed early onset
- 1 first-degree relative with prostate cancer then 2x risk
- Increasing AGE
- AFRO-CARIBBEAN ethnicity
Presentation of Prostate cancer
- LUTS (same as BPH)
- Systemic cancer symptoms
- UNEXPLAINED WEIGHT LOSS
- Fatigue
- NIGHT PAIN
- Haematuria - may indicate metastasis
- BONE PAIN (indicates METASTASIS)
- Typically LUMBAR BACK PAIN
What kind of bone lesions does prostate cancer cause
SCLEROTIC LESIONS
- thick, looks white on x-rays
Which areas does prostate cancer typically metastesise to
- lymph nodes
- BONE (particularly sacrum due to interconnected blood flow)
- Liver
- Lung
- Brain
Diagnosis of prostate cancer
In community:
- DRE - can feel HARD, IRREGULAR (nodules)
- PSA test (non-specific to cancer + normal levels vary from person to person)
- TRANSRECTAL ULTRASOUND w/ BIOPSY (DIAGNOSTIC)
- US scan and Biopsy can also be done seperately, Biopsy is the GS
What grading system is used for prostate cancer
Gleason score
- Low = <= 6
- Intermediate = 7
- High/v. high:
- Grade group 4 = Gleason score 8
- Grade group 5 = Gleason score 9-10
It is worked out based on histological pattern of cells as they progress from normal to cancerous. Resembles normal = grade 1; So mutated they barely resemble normal = grade 5.
- Pathologist identifies the 2 most prominant types of cancer cells in biopsy and adds them together to give overall Gleason score
Treatment of prostate cancer
- If local - PROSTATECTOMY
- If metastatic (surgical/medical castration)
- HORMONE THERAPY (prostate growth is stimulated by testosterone/DHT so reduced hormones = reduced cancer growth)
- GnRH AGONISTS (stops LH/FSH productions by continuously stimulating pituitary -> overcomes pulsatile GnRH release - exogenous suppression of HPG axis) - most common med
- GOSERELIN or ZOLADEX (SE - erectile dysfunction, loss of libido etc.)
- Bilateral orchiectomy (castration - removes testes) - v. effective (remission)
- GnRH AGONISTS (stops LH/FSH productions by continuously stimulating pituitary -> overcomes pulsatile GnRH release - exogenous suppression of HPG axis) - most common med
- HORMONE THERAPY (prostate growth is stimulated by testosterone/DHT so reduced hormones = reduced cancer growth)
- CHEMO/RADIOTHERAPY (typically Radiotherapy) - DOCETAXEL CHEMO (alongside castration if fit enough)
- Abiraterone (androgen receptor targeted - alongside castration if not fit enough for chemo)
If progresses to castration-resistant disease:
- 2nd line androgen receptor targeted hormone therapy:
- Abiraterone
- Enzalutamide
- Further Cytotoxic chemotherapy: Docetaxel, Carbazitaxel
- Bisphosphonates: Zoledronic Acid
- Palliation - castration-resistant = high mortality
- need to account for :
- pain
- spinal cord compression
- uretric obstruction
- anaemia
- need to account for :
Cryotherapy is also an option (i would assume for more localised cancer)
Often SLOW GROWING so may just do WATCHFUL WAITING (esp if older)
Define what a UTI is
The presence of microorganisms in the urinary tract which produces CLINICAL FEATURES.
It can affect the lower tract causing cystitis (bladder), urethritis and prostatitis, and the upper causing pyelonephritis. It can also occur from untreated urolithiasis
What are the 5 most common pathogens that cause UTIs
Remember with KEEPS:
- Klebsiella
- E coli- most common causing >50% of cases (UPEC - uropathogenic e coli)
- Enterococci
- Proteus spp
- Staphylococcus coagulase negative (NOT staph aureus) - SAPROPHYTICUS
What are the storing LUTS commonly seen in UTIs
Remember FUND
- Frequency
- Urgency
- Nocturia
- Dysuria
Define Pyelonephritis
infection and inflammation of the RENAL PARENCHYMA, soft tissues of RENAL PELVIS + UPPER URETER
- most often due to ascending UTI from own bowel flora (esp E COLI)
- can also infect via blood/lymph - associated with SEPSIS
Risk factor for UTIs in general
FEMALE - shorter urethra - closer to anus - easier for bacteria to colonise (+ INFANTS)
ELDERLY esp CATHETERISED/INSTITUTIONALISED
Risk factors/causes for Pyelonephritis
- Urine stasis (stones or BPH)
- Renal structural abnormalities
- Catheters
- Diabetes
- Pregnancy
- Immunocompromised
Particularly affects FEMALES under 35 yrs
Caused by ASCENDING UTI (bacteria move up from urethra); HAEMATOGENOUS spread of pathogens (via blood - esp S. AUREUS, CANDIDA); Lymphatic spread
Presentation of Pyelonephritis
May be asymp
- Classic triad of symptoms:
- LOIN PAIN
- FEVER
(- N+V) - PYURIA (WBC + PUS in urine) on investigation
- May get Haematuria
- Costovertebral joint/RENAL ANGLE TENDERNESS/pain
- Rigors
- Significant bacteriuria
Oliguria if it causes AKI
Septic shock in advanced disease
Investigations for Pyelonephritis
- ABDO EXAM
- Tender loins + renal angle tenderness (+ rule out outher abdo pathology)
- BLOODS - elevated inflam markers
- URINALYSIS/URINE DIPSTICK
- white cells; Nitrites (bacteria break down nitrates -> nitrites); microscopic haematuria (protein)
- leucocyte elastase
- foul smelling
- MID STREAM URINE SAMPLE, CULTURE + MICROSCOPY (gold - diagnostic)
RENAL/UPPER TRACT USS - to rule out urinary tract obstruction or stones, abnormal anatomy, incomplete bladder emptying
Treatment for pyelonephritis + Complications
Rest
FLUID REPLACEMENT (Cranberry juice?, lots of water)
ANALGESIA (paracetamol NOT opiods)
Antibiotics (BROAD SPECTRUM):
- CIPROFLOXACIN or CO-AMOXICLAV (both ORAL)
- IV GENTAMICIN or CO-AMOXICLAV if SEVERE
- CEFALEXIN for 7-10 days if PREG
- Trimethoprim or amoxicillin if sensitive.
Surgery to drain abscesses/remove calculi if required
- May need catheter
If CHRONIC -> NEPHRECTOMY
Complications:
- Renal abscess
- Emphysematous pyelonephritis (Gas accumulation in renal parenchyma, collecting system or perinephritic tissue due to necrotizing infection of renal parenchyma)
- Kidney fibrosis
- Sepsis
Define Cystitis
Infection of the urinary bladder
- it is most common in young sexually active women
Oft a UPEC (uropathogenic e coli) infection
Risk factors for Cystitis
- Urine stasis (from obstruction)/poor emptying
- Catheters
- Bladder epithelium damage
History of UTI
Diabetes
Frequent sexual intercourse?
Pregnancy
Presentation of Cystitis
- Dysuria- discomfort, pain, burning on urination
- Frequency
- Urgency
- Cloudy smelly urine
- Haematuria
-
Suprapubic tenderness/discomfort
- abdo/loin as well potentially
Diagnosis of Cystitis
Urine dipstick- if positive for nitrites or WBCs and RBCs then UTI likely
- unreliable in women over 65 so don’t bother
MID STREAM Urine Microscopy, culture and sensitivity (gold)
Management of Cystitis
Antibiotics:
- 3 days of TRIMETHOPRIM, or NITROFURANTOIN or CEFALEXIN.
- avoid nitrofurantoin at TERM in pregnancy.
- TRIMETHOPRIM CONTRAINDICATED in pregnancy
- 2nd LINE = CIPROFLOXACIN or Co-AMOXICLAV
- amoxicilin if pregnant
Causes of Urethritis
Usually a SEXUALLY ACQUIRED INFECTION
- Non-gonococcal:
- CHLAMYDIA TRACHOMATIS (main - esp 15-24 y/o)
- Mycoplasma genitalium
- Ureaplasma urealyticum
- Trichomonas vaginalis
- Gonococcal: NESSERIA GONORRHOEA (less common)
Non-infective cause = Trauma, stricture, irritation, stones
Risk factors for Urethritis
UNPROTECTED SEX
- MSM esp
male
Presentation of Urethritis/common STIs
- DYSURIA +/- URETHRAL DISCHARGE (blood/pus)
- Urethral pain
- penile discomfort
- potential skin lesions
- may get systemic symptoms
Chlamydia:
- Men = TESTICULAR pain
- Voiding symptoms, dysuria
- 50% asymp
- Women = VAGINAL discharge and dysuria
- white, yellow or green discharge
- 70% are asymp
Gonorrhoea:
- more LIKELY to be ASYMP (90-95%)
- Men = dysuria, frequency, discharge
- Women = VAGINAL discharge, dysuria, PELVIC pain
Diagnosis of Urethritis
- NAAT (nucleic acid amplification test) - GOLD
- Detects STI if present
- Female - SELF COLLECTED VAGINAL SWAB (best), endocervical swab, first void urine
- Male - FIRST VOID URINE
- URINALYSIS/DIP STICK (to exclude UTI)
- Blood cultures
(??- MID STREAM CULTURE + SENSITIVITY)
For Gonorrhoea - need to SWAB infected areas and CULTURE/MICROSCOPY
- urethral smear
Treatment of Urethritis
- N. Gonorrhoea:
- single IM CEFTRIAXONE dose + ORAL AZITHROMYCIN
- partner notification, patient education + contact tracing
- C. Trachomatis:
- Single dose of 1g AZITHROMYCIN
- 7 days of DOXYCYCLIN (bi-daily)
- test for other STIs
- avoid sex till finished + contact tracing
- If PREGNANT:
- ORAL ERYTHROMYCIN 14 days
- or ORAL AZITHROMYCIN STAT
What condition is urethritis often linked to
REACTIVE ARTHRITIS
- Can’t see, can’t pee, can’t climb a tree
- conjunctivitis, urethritis, arthritis
Define Epididymo-Orchitis + it’s aetiology + risk factors
Inflammation of epididymus extending to testes
- Usually due to urethritis (STI) or MAINLY Extension of Cystitis (KEEPS)
Most common in MALE 15-30 yrs (STIs) and OVER 60s (KEEPS - UTIs)
Also: MUMPS, TRAUMA, CATHETER in ELDERLY
RFx:
- Previous infection
- Indwelling catheter
- Structural/functional abnormality of urinary tract
- Anal intercourse (MSM esp)