Urology Flashcards
Function of the Urinary Tract
To collect urine produced continuously by the kidneys
To store collected urine safely
To expel urine when socially acceptable
Anatomy of kidney
Retroperitoneal organs
Lie between T11 – L3
Blood supply from renal artery direct from aorta at L1 level
How many nephrons does each kidney contain
1 million nephrons
How much urine does each kidney produce a day
1-1.5L of urine per day
Ureters- Anatomy
25cm – 30cm
Retroperitoneal organs
Run over psoas muscle, cross the iliac vessels at the pelvic brim and insert into trigone of bladder
Ureters function
Transport urine from the kidney to the bladder via peristalsis
What is preventing the reflex of urine
a valvular mechanism at the vesicoureteric junction
Nervous Control of the Bladder and Sphincter- 4 nerve
Parasympathetic Nerve (pelvic nerve)
Sympathetic Nerves (hypogastric plexus)
Somatic Nerve (pudendal nerve)
Afferent pelvic nerve
Nervous Control of the Bladder and Sphincter- Parasympathetic Nerve (pelvic nerve)
- S2-S4
- acetylcholine neurotransmitter
- involuntary control
Nervous Control of the Bladder and Sphincter- Sympathetic Nerves (hypogastric plexus)
T11 – L2
noradrenaline neurotransmitter
involuntary control
Nervous Control of the Bladder and Sphincter- Somatic Nerve (pudendal nerve)
S2-S4
“Onuf’s nucleus”
acetylcholine neurotransmitter
Nervous Control of the Bladder and Sphincter- Afferent pelvic nerve
Sensory nerve
signals from detrusor muscle
Neural Control- Onuf’s Nucleus
Responsible for guarding reflex
Neural Control- Pontine Micturition Centre/Periaqueductal Grey
Responsible for Co-ordination of voiding
Neural Control- Cortex
Responsible for voluntary control
Neural Control- Sacral Micturition Centre
Responsible for Micturition reflex
Storage Phase
Bladder fills continuously
As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance
Filling Phase
At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord
Filling phase- nerves
-Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation
-Somatic (Pudendal) nerve stimulation maintains urethral contraction
Voiding Phase – Micturition Reflex
Autonomic spinal reflex
Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord
Voiding Phase – Micturition Reflex- nerves
Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts
Pudendal nerve is inhibited and the external sphincter relaxes
Guarding Reflex
Voluntary control of micturition
Guarding Reflex
Afferent signals from the pelvic nerve are received by the PMC/PAG 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
Storage summary
Receptive Relaxation
Detrusor relaxation (sympathetic stimulation T11-L2)
External Urethral Sphincter contracted (pudendal stimulation S2-4)
Micturition
Voluntary control from cortex and PMC
Detrusor contraction (parasympathetic stimulation S2-4)
External Urethral Sphincter relaxation (pudendal inhibition S2-4)
Penile cancer epidemiology
Rare in UK, more common in far east and Africa
Very rare in circumcised
Related to smegma, chronic inflammation and viruses
Penile cancer presentation
Chronic fungating ulcer, bloody/purulent discharge
50% spread to lymph at presentation
Penile cancer treatment
Radiotherapy and iridium wires (protons instead of x-ray radiation) if early
Amputation and lymph node dissection if late
Benign diseases of the penis
Balanitis, Phimosis, Paraphimosis
Balanitis
Acute inflammation of the foreskin and glans
Association with strep and strap infections
More common in diabetes and young children with tight foreskins
Balanitis- treatment
Antibiotics, circumcision, hygiene advice
Phimosis
Foreskin occludes the meatus (hole where fluids leave body)
Young boys- recurrent balanitis + ballooning, may heal with time or require circumcision
Adult- presents with painful intercourse, infection, ulceration
Paraphimosis treatment
Ask patient to squeeze glans
Try applying 50% glucose-soaked swab (oedema may follow osmotic gradient), ice packs and lidocaine gel may help
May require aspiration, dorsal slit, circumcision
Paraphimosis
Occurs when tight foreskin is retracted and becomes irreplaceable, preventing to venous return leading to oedema and even ischemia of the glans
Can occur if the foreskin is not replaced after catheterization
Impotence
Erectile dysfunction
Common in over 50s
Physiological facet is common
Normal erection function
Results from neuronal release of NO which, via cGMP and Ca2+, hyperpolarizes and thus relaxes vascular and trabecular smooth muscle cells, allowing engorgement
Impotence causes
Physiological
Organic- Big 3- smoking, alcohol + diabetes
- Endocrine, neurological, pelvic surgery, radiotherapy, atheroma, renal/ hepatic failure, prostatic hyperplasia, penile abnormalities, drugs
Impotence investigations
Full sexual and physiological work up
Bloods- U+E, LFTs, glucose, TFT, LH, FSH, lipids, testosterone, prolactin
Doppler test (US to see how blood flows in the penis during and after an erection)
Impotence treatment
Treat underlying causes
Counselling
Oral phosphodiesterase inhibitors (increase cGMP)
Bladder tumours
In the UK >90% are transitional cell carcinomas
Adenocarcinomas and squamous cell carcinomas are rare in west
More common in men then women
Bladder tumours- grading
Grade 1- differentiated
Grade 2- intermediate
Grade 3- poorly differentiated
Bladder tumours- location
80% confined to bladder mucosa
20% penetrate muscle (worse prognosis)
Bladder tumour- presentation
Painless haematuria (blood in urine), recurrent UTIs, voiding irritability
Bladder tumour- associations
Smoking, aromatic amines (rubber industry), chronic cystitis schistosomiasis, pelvic irradiation
Bladder tumour- investigations
Cystoscopy with biopsy is diagnostic
CT urogram is diagnostic (provides staging)
Urine- microscopy/cytology
MRI/ lymphangiography may show involved nodes
Bladder tumour- staging Tis
Carcinoma in situ
Bladder tumour- staging Ta
Tumour confined to epithelium
Bladder tumour- staging T2
Invades muscle
Bladder tumour- staging T1
Tumour in submucosa or lamina propira
Bladder tumour- staging T3
Extends to perivesical fat
Bladder tumour- staging T4
Invades adjacent organs
Bladder tumour- staging N0-N4
N0- no lymph node involvement
N1-N4 progressive lymph node involvement
Bladder tumour- staging M0/M1
M0- no mets
M1- distant mets
Treatment of transitional cell carcinomas (TCC) of the bladder- Tis/Ta/T1
80% of all patients
Diathermy (deep heating) via transurethral cystoscopy or TURBT (transurethral resection of bladder tumour)
Consider intravesical BCG (stimulates a non specific immune response)
Treatment of transitional cell carcinomas (TCC) of the bladder- T2-3
Radical cystectomy (removal of bladder) is gold standard
Radiotherapy gives worse survival rates but preserves the bladder
Post-op chemo toxic but effective
Trying other surgical methods to preserve the bladder, but none are effective yet
Treatment of transitional cell carcinomas (TCC) of the bladder- T4
Usually palliative chemo/radiotherapy
Chronic catheterization and urinary diversions may help relive pain
What to use to measure chronic disease
eGFR and ACR (albumin to creatinine ratio)
Chronic kidney disease- prevalence in UK
4.19%, large differences in areas due to difference in age, health inequality
Most common cause of end stage kidney disease in the UK
Diabetes (diabetic neuropathy)
Other common causes- hypertension, glomerulonephritis, secondary to pre-eclampsia
Blood pressure control in CKD
High protein in urine= lower BP threshold for hypertension intervention
ACEi/ARBs are first line
Diabetic Nephropathy in CKD
Hyperglycaemia leads to increase in growth factors, RAAS activation and oxidative stress. This causes increase in glomerular capillary pressure, podocyte damage and endothelial dysfunction.
Albuminuria is 1st clinical sign, later scarring (glomerulosclerosis), nodule formation, and fibrosis with progressive loss of renal function ie CKD
Anaemia in CKD
Common as EPO is produced in peritubular cells of the kidney, when kidneys are damaged, EPO production reduces
Less EPO, less RBC production, less O2
Fluid overload in CKD
Progressive loss of renal function causes reduced sodium filtration and inappropriate suppression of tubular reabsorption that ultimately lead to volume expansion
Sodium in CKD
Sodium accumulation is one of the consequences of renal failure, resulting in increased water intake, increases in the extracellular volume, and accompanying rise in blood pressure
Most common cause of death with CKD
Cardiovascular events
Glomerulonephritis in CKD
inflammation of the glomeruli. Severe or prolonged inflammation associated with glomerulonephritis can damage the kidneys causing CKD
SGLT2 inhibitors in CKD
effective at slowing the progression of kidney disease, reducing heart failure, and lowering the risk of kidney failure and death in people with CKD and type 2 diabetes
Bone mineral disorders in CKD
Damaged kidneys stop
-turning vitamin D into calcitriol, creating an imbalance of Ca2+ in your blood
-removing excess phosphorus from your blood, triggering your blood to pull Ca2+ out of your bones and causing them to weaken
-release extra PTH, Ca2+ from your bones to restore your blood calcium levels
Who gets renal cancer?
Hypertension, obesity, smoking- (oxidative stress)
Other renal cancer RF
family history (5%- VHL usually)
ESRF
Tuberous sclerosis
Renal cancer investigation
Flank pain, palpable mass, blood in urine- classic trifecta
Imaging- CT, MRI
Horse shoe kidney
a condition in which the kidneys are fused together at the lower end or base
Haematuria and 2 week wait guidance
Visible Haematuria, over 45%, 30% risk of cancer
Non-visible haematuria, over 60, 5% risk of cancer
Cannonball metastases
Classic feature of metastatic renal cell carcinoma, appears as clearly defined circular opacites scattered throughout the lung
Most common renal cancer type
Clear cell renal carcinoma
Others- papillary and chromophobe carcinomas
Treatment options for renal cancer- surgical
Radical/partial nephrectomy, to remove tumour is first line
Treatment options for renal cancer- non invasive
Arterial embolisation- cutting off the blood supply to the affected kidney
Percutaneous cryotherapy- injecting liquid nitrogen to freeze and kill the tumour cells
Radiofrequency ablation- putting a needle in the tumour and using an electrical current to kill the tumour cells
GFR influenced by
Net Filtration Pressure (NFP)- Hydrostatic pressures + Colloid osmotic pressures
Renal Blood Flow (RBF)- Autoregulation
Filtration coefficient
4 starling forces effecting net fluid movement
Glomerular hydrostatic pressure- fluid out
Bowman’s Capsule fluid pressure- fluid in
Glomerular colloid osmotic pressure
(pi*G; protein)- fluid in
Bowman’s Capsule colloid osmotic pressure- should be negligible as albumen is filtered out
Net Filtration Pressure (NFP) =
Glomerular hydrostatic pressure - (Bowman’s Capsule fluid pressure + Glomerular colloid osmotic pressure)
Renal Auto-regulation
Intrinsic feedback mechanisms
-Afferent and efferent arterioles
-Tubuloglomerular Feedback
Why is creatine used to measure eGFR
Production rate is roughly similar to clearance rate in the body
GFR equation
urine flow rate * [creatine] urine] / [creatine] plasma
Problems with eGFR
Doesn’t consider creatinine tubular secretion
Significant decrease GFR small [Cr] plasma- Need several time points
Creatinine metabolism reflection on lean body mass
Not valid in pregnancy
DAMN drugs
Induce, exacerbate or complicate AKI: acidosis, hypovolaemia or hypertension
DAMN drugs- acronym meaning
Diuretics
ACEis/ARB
Metformin
NSAIDs
Factors that Decrease GFR
Increase Afferent artery resistance- NSAIDs
Decrease efferent artery resistance, decrease angiotensin II (ACEi/ARB)
Increase Glomerular colloid osmotic pressure- decrease renal BF, increase plasma proteins
Increase bowmens c
Factors that Decrease GFR- increase Afferent artery resistance
NSAIDs
Factors that Decrease GFR- decrease Efferent artery resistance
Due to decrease Angiotensin II ie ACEi/ARB
Factors that Decrease GFR- increase Glomerular colloid osmotic pressure
Decrease in renal BF, increase in plasma protein
Factors that Decrease GFR- increase Bowmen capsule fluid pressure
Urinary tract obstruction (kidney stones)
Factors that Decrease GFR- decrease kidney function
Renal disease Diabetes mellitus Hypertension
Factors that Decrease GFR- decrease Glomerular hydrostatic pressure
Decrease Arterial pressure (small effect)
Which ion has a key role in determining plasma volume and osmolality?
Na+
Expansion of Fluid Volume - A Simple System
Increase Blood volume
Increase BP
Increase renal excretion
Normal vol restored
Regulation of Blood Pressure and Volume
Baroreceptor reflexes (medulla)- measure BP
Osmoreceptor Reflexes (hypothalamus)- measure Na+
Pressure Natriuresis and Atrial Natriuretic Peptide (ANP)
ANP generally antagonises Angiotensin-II actions
- inhibits renin secretion
-afferent arteriole dilation
Benign prostatic hyperplasia- epidemiology
Very common
24% for 40-64
40% for 64+
Benign prostatic hyperplasia- pathology
Benign nodular or diffuse proliferation of musculofibrous and glandular layers
Inner (transitional) zone enlarges
Benign prostatic hyperplasia vs prostate carcinoma- pathology
Benign prostatic hyperplasia- Inner (transitional) zone enlarges
Prostate carcinoma- enlargement of peripheral layers of the prostate
Benign prostatic hyperplasia- presentation
LUTS (lower urinary tract symptoms)
LUTS (lower urinary tract symptoms)
Nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria, bladder stones, UTIs
Benign prostatic hyperplasia- tests
MSU (Midstream Specimen of Urine), U+Es, Ultrasound, PSA (prostate-specific antigen), transrectal ultrasound +/- biopsy
PSA (prostate-specific antigen)
A protein produced by both cancerous and noncancerous tissue in the prostate
Benign prostatic hyperplasia- lifestyle management
Avoid alcohol, caffeine
Relax when voiding, void twice to aid emptying
Train bladder by practising distraction methods and holding on
Benign prostatic hyperplasia- drug management
Alpha-blockers are 1st line (decrease smooth muscle tone)
5 alpha-reductase inhibitors- shrink the prostate gland if it’s enlarged, can be used alone or in combination
Benign prostatic hyperplasia- surgical indications
Have complications attributed to BPH, such as acute and/or chronic renal insufficiency, recurrent bladder stones, gross recurrent haematuria, recurrent UTIs
Have refractory responses to medication
Benign prostatic hyperplasia- surgical management
Transurethral resection of the prostate (TURP)- historical standard
Other options- Simple prostatectomy, Transurethral vaporisation of the prostate (TUVP)
Glomerulonephritis
Group of diseases that cause inflammation and damage to glomeruli
May be acute or chronic
Glomerulonephritis Signs/symptoms
Declining renal function
Hypertension
Leaky glomerulus- haematuria, proteinuria
Glomerulonephritis Progression
Causes 25% of ESKF
Glomerulonephritis Pathophysiology
Glomerulonephritis is usually immunologically mediated:
-Immunoglobulin deposits
-Inflammatory cells
-Response to immunosuppressive therapy
Acute Nephritic syndrome- characteristics
Acute kidney injury, active dipstick (haematuria and proteinuria), Oliguria, hypertension and fluid overload
Acute Nephritic syndrome- immune mediated examples
ANCA associated vasculitis
Goodpasture’s disease, SLE (systemic lupus erythematosus), systemic sclerosis, post-streptococcal infection, Crescentic IgA nephropathy, Henoch Schonlein purpura (HSP)
Acute Nephritic syndrome - Urine
Haematuria key feature- red ell casts on urine microscopy characteristic of glomerular bleeding
Proteinuria is variable but usually sub-nephrotic levels
Acute Nephritic syndrome - Hypertension
Hypertension common
Can be severe and present as hypertensive emergency
Risk of stroke, retinopathy, MI
Acute Nephritic syndrome - Fluid
Fluid retention often seen
Signs/symptoms
- Hypertension
- Pulmonary oedema/effusions
- Peripheral oedema
- Raised JVP
-Orthopnea and Shortness of Breath
-Increasing weight
ANCA-Associated Vasculitis
ANCA = antineutrophil cytoplasmic antibodies
Multisystem small vessel vasculitis
Vasculitis
Inflammation of blood vessels
ANCA-Associated Vasculitis- treatment
Immunosuppression: steroids, cyclophosphamide, rituximab, (plasma exchange)
ANCA-Associated Vasculitis (ANCA-AAV) Features
systemic inflammatory features
Features of other organ system involvement.
Greater incidence in white and 50-79
ANCA-Associated Vasculitis (ANCA-AAV)- investigation
Serum ANCA
Changes in ANCA titre correlate with disease activity
Biopsy of glomerulus
ANCA-Associated Vasculitis (ANCA-AAV)- biopsy
Segmental glomerular necrosis with crescent formation. Degree of active lesions, fibrosis and tubular atrophy are important prognostic markers.
IgA Nephropathy
Abnormality in IgA glycosylation leads to deposition in mesangium (close proximity to glomerulus)
May run a benign, insidious or aggressive course
Overlap with HSP (Systemic form)
Commonest cause of glomerulonephritis world wide
Systemic Lupus Erythematosus (SLE)
autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage
Systemic Lupus Erythematosus (SLE)- signs and symptoms
Rash, arthralgia, kidney failure, neurological symptoms, pericarditis, pneomonitis
Systemic Lupus Erythematosus (SLE) - Treatment
Immunosuppression – steroids, cyclophosphamide, mycophenolate mofetil, rituximab
Systemic Sclerosis
rare chronic disease of unknown cause characterized by diffuse fibrosis and vascular abnormalities in the skin, joints, and internal organs
Anti- glomerular Basement Membrane disease (Goodpasture syndrome)
Autoimmune destruction of own collagen, affects alveoli and glomerulus primary
Anti- glomerular Basement Membrane disease (Goodpasture syndrome)- clinicals signs
Rapidly progressive kidney failure, active dipstick. Haemoptysis
Anti- glomerular Basement Membrane disease (Goodpasture syndrome)- treatment
remove antibody
-plasma exchange, immunosuppression -steroids/ cyclophosphamide
Henoch Schonlein purpura (HSP)
Systemic form of IgA Nephropathy
More commonly children, often provoked by URTI
Henoch Schonlein purpura (HSP)- clinical signs
Triad of: Purpuric rash, abdominal pain, acute kidney injury (IgA deposition on kidney biopsy)
Nephrotic syndrome- clinical signs
Triad of heavy proteinuria, hypoalbuminemia, oedema
Other feature- Hypercholesterolaemia
- Haematuria usually absent or mild
Common causes of nephrotic syndrome- primary
Minimal change – children+ adults
Membranous – caucasian adults
Focal Segmental Glomerulosclerosis – adults
Common causes of nephrotic syndrome- secondary
Diabetes
Amyloid (usually AL)
Infections
SLE
Drugs – gold, penicillamine
Malignancy
Management Nephrotic Syndrome
Establish Cause – renal biopsy usually required
Treat complications – manage fluid state
Treat underlying cause
Nephrotic Syndrome- Investigations
Serum albumin, creatinine (+eGFR), lipids and glucose, urinalysis
Urine protein creatinine ratio – to quantify proteinuria
Nephrotic Syndrome- supportive treatment
Control fluid state – diuretics, ACEi/ARBs, spironolactone
Statins
Anticoagulation
Prevent infections – prophylactic antibiotics in children
Membranous Nephropathy
Thickening of glomerular capillary wall. IgG, complement deposit in sub epithelial surface causing leaky glomerulus
Membranous Nephropathy- clinical features
nephrotic syndrome (Nephrotic range proteinuria, hypoalbuminemia and oedema)
Membranous Nephropathy- diagnosis
serum PLA2R Ab, look for secondary causes, renal biopsy
Membranous Nephropathy- natural history
10yr renal survival of 100% in those who achieve complete remission, 90% with partial remission and only 45% with no remission
30% spontaneous remission
Membranous Nephropathy- treatment
Depends on risk
Wait and see for low risk
Steroid therapy for higher risk
Minimal Change Disease
biopsy appears normal on light microscopy but fused podocytes on electron microscopy
Often in children or younger patients, does have spike in incidence at older ages
Minimal Change disease- treatment
Steroids is first line
Asymptomatic urinary abnormalities
Incidental finding of dipstick haematuria +/- proteinuria
Kidney function and blood pressure normal
Asymptomatic urinary abnormalities common causes
IgA, Thin membrane disease
Asymptomatic urinary abnormalities- diagnosis
usually clinical – don’t biopsy unless kidney function abnormal or significant proteinuria
Thin membrane disease
Often inherited – may affect 1% of population
Probable benign and indolent natural history
Often genetic cause: Type IV collagen variants
Glomerulonephritis- CKD causes
IgA nephropathy, membranous, diabetes, mesangiocapillary GN, HIV associated nephropathy, Alports
Alports syndrome
genetic condition characterized by kidney disease, loss of hearing, and eye abnormalities caused by mutation in Type IV collagen
X-linked inheritance
Alports Syndrome- features
-Renal: Progressive CKD, Haematuria, proteinuria
-Sensorineural Hearing loss
-Can develop nephrotic syndrome
Prostate cancer
Commonest male malignancy
Incidence increase with age, 80% in men over 80
Prostate cancer- pathophysiology
Most are adenocarcinomas arsing in peripheral
Spread may be local (seminal vesicles, bladder, rectum), via lymph or haematogenously (sclerotic bone lesions)
Prostate cancer- symptoms
Asymptomatic or urinary retention, poor stream, frequency, and nocturia
Weight loss +/- bone pain suggest mets
Prostate cancer- investigations
Prostate exam- hard, irregular prostate
High PSA
Transrectal US and biopsy (required for diagnosis), CT, MRI (for staging)
Prostate cancer- treatment approach
Treatment decision depends on risk group, life expectancy and patient preference
Ranges from wait and see to androgen deprivation therapy (ADT), external beam radiotherapy (EBRT), brachytherapy to radical prostatectomy
Prostate cancer- Androgen deprivation therapy (ADT)
Androgen deprivation may be achieved medically, with a luteinising hormone-releasing hormone (LHRH) agonist or antagonist, or by surgical castration (bilateral orchiectomy)
Prostate cancer- Radical prostatectomy
Option when when the tumour is confined to the prostate and life expectancy is ≥10 years,
Prostate cancer- Observation
Monitoring progression of symptoms, PSA levels and biopsies (active surveillance)
PSA (prostate-specific antigen)
Serum PSA levels may be increased in patients with prostate cancer; however, other non-malignant conditions (e.g., prostatitis and benign prostatic hyperplasia) may increase PSA levels.
PSA levels may also vary according to race
Acute kidney injury
Syndrome of decreased renal function, measured by serum creatine or urine output, occurring over hours-days
Acute kidney injury- definition
Rise in creatine > 26 micromol/L within 48 hours
Rise in creatine >1.5x the baseline over a week
Urine output <0.5 mL/kg/h for 6 consecutive hours
Acute kidney injury- pre renal
Decrease in blood volume and blood flow –> decrease in effective arterial blood volume
Acute kidney injury- pre renal causes
hypovolemia of any cause
heart, liver, kidney failure
sepsis
emboli
RAS
Drugs NSAIDs, Tacrolimus, ACE I
Hyper Ca
Acute kidney injury- pre renal causes- low cardiac output
Low CO> decrease in mean arterial pressure > increase in art renal resistance > decrease in eGFR > rise in serum Cr
Acute kidney injury- pre renal causes- low albumin states
Low albumin states > low oncotic pressure > fluid in 3rd space > low mean arterial pressure > decrease in eGFR > rise in serum Cr
Acute kidney injury- pre renal causes- increased permeability of vessels
Systemic vasodilation > fluid in 3rd space > decrease mean arterial pressure > decrease in eGFR > rise in serum Cr
Acute kidney injury- intra renal
a disease process causes damage to the kidney itself resulting in AKI
Acute kidney injury- intra renal causes
Acute tubular necrosis, Acute interstitial nephritis, Glomerulonephritis, Hypertension, thrombotic microangiopathies
Acute kidney injury- intra renal- acute tubular necrosis causes
Low blood pressure
Drugs: aminoglycoside, vancomycin, acyclovir
Contrast
Hemolysis, rhabdomyolysis, tumor lysis
Acute kidney injury- intra renal- Acute interstitial nephritis causes
Drugs: abx, PPI
infections
SLE, sarcoidosis
Acute kidney injury- intra renal-thrombotic microangiopathies
thrombotic thrombocytopenic purpura (TTP), haemolytic uremic syndrome (HUS) and Disseminated intravascular coagulation (DIC)
Acute kidney injury- post renal- pathology causes
Within renal tract or extrinsic compression
Acute kidney injury- post renal- within renal tract causes
Stone, renal tract malignancy, stricture, clot
Acute kidney injury- post renal- extrinsic compression causes
Pelvic malignancy, prostatic hypertrophy, retroperitoneal fibrosis
Acute kidney injury- diagnosis investigations
Urine Cr, urine dip, urine osmolality, urine Na, Ultrasound of the Kidneys, Ureters & Bladder (KUB)
Acute kidney injury- signs
Azotaemia, hyperkalaemia, decrease urine output, fluid overload, accumulation of drugs
Azotaemia
biochemical abnormality- elevation, or build up of nitrogenous products, creatinine in the blood, and other secondary waste products within the body
Acute tubular necrosis- urine dip
Muddy brown casts
Eosinophils
Urinary casts
Tiny tube-shaped particles that can be found when urine is examined under the microscope during a test called urinalysis
Acute kidney injury- management principles
Supportive therapy with close ongoing monitoring
Identification and management of the underlying cause (sepsis, nephrotoxic medication, urinary tract obstruction)
Recognition and correction of life-threatening complications (hyperkalaemia, acidosis, volume overload)
Acute kidney injury-indications for dialysis
HyperK
Uraemia
Acidosis
Intoxication
Fluid overload
Acute kidney injury- complications
Hyperkalaemia, Acidosis, Pulmonary oedema
Acute kidney injury- Fluids principles
Resuscitation, replacement, maintenance
Acute kidney injury- STOP AKI
Sepsis, Toxins, Optimise volume status/BP, Prevent harm
UTI
Combination of clinical features and the presence of bacteria in the urine
Lower tract UTI
Bladder (cystitis), prostate (prostatitis)
Lower tract UTI
Pyelonephritis= infection of kidney/ renal pelvis
UTI classifications
Complicated, Uncomplicated, Asymptomatic bacteriuria
Complicated UTI
Structural/functional abnormalities of the GU tract ie obstruction, catheter, stones, neurogenic bladder, renal transplant
Common in pregnant, men, catheterised, children, immunocompromised
Uncomplicated UTI
Normal renal tract structure and function
Non-pregnant women
Most common cause of UTI
E. coli
UTI organisms
Usually anaerobes and gram-negative bacteria from bowel and vaginal flora
UTI organism examples
E. coli, Staph. saprophyticus, Proteus and Klebsiella
UTI causes- ureters
Stasis during pregnancy, Ureteric stones, Proteus (produces urease, increase pH, stone formation
UTI causes- bladder
Ureteric reflex, low urinary vol, bladder stones/tumour, E. coli fimbriae for bladder colonisation, obstruction from prostatic hypertrophy
UTI causes- urethra
Bowel flora -> female shot urethra
Catheterisation allowing colonisation
UTI symptoms- Cystitis
Frequency, dysuria, urgency, suprapubic pain, polyuria, haematuria
UTI symptoms- Acute pyelonephritis
Classic triad- loin pain, fever, pyuria
Others- rigor, vomiting, costovertebral pain, associated cystitis symptoms, septic shock
UTI symptoms- Prostatitis
Pain in periunem, scrotum, penis, bladder, lower back
Fever, malaise, nausea, urinary symptoms, swollen or tender prostate on DRE
UTI clinical signs
Fever, abdominal or loin pain
Check for distended bladder, enlarged prostate
Differential for vaginal discharge
Pelvic inflammatory disease
Pelvic inflammatory disease
infection of the female reproductive system which includes the womb, fallopian tubes and ovaries.
UTI first order investigations
Urine dipstick, Urine culture and sensitivity (MSU)
UTI- urine dipstick test
Useful in unpregnant women <65
Positive for nitrite and leukocytes
Can be negative and still be a UTI
UTI- Urine culture and sensitivity (MSU)
Use in pregnant women, men, children, not responding to empirical antibiotic
UTI key diagnostic symptoms
dysuria, new nocturia, or cloudy-looking urine
UTI- further investigations
Bloods- FBC, U+E, CRP and blood culture (if systemically unwell)
Imaging- USS and cystoscopy/ urodynamics/ CT
UTI asymptomatic bacteriuria management
Do not use antibiotics for non pregnant women, men and adults with catheters
Treat pregnant women immediately with antibiotics
Lower UTI management- Non pregnant women
3 day course of empirical antibiotics
Supportive care- fluids, paracetamol or ibuprofen for pain relief
Culture urine and pathogen-targeted antibiotic if empirical treatment fails
Empirical antibiotics for lower UTI treatment
Trimethoprim
Nitrofurantoin if eGFR ≥45 mL/minute
Upper UTI management- Non pregnant women
Urine culture
Treat initially with broad spectrum antibiotics
Consider hospitalisation if antibiotic resistant
Empirical antibiotics for Upper UTI treatment
Amoxicillin/clavulanate (if culture results are available due to high resistance rates)
Cefuroxime
Ceftriaxone
Ciprofloxacin
Gentamicin or amikacin
UTI- management in pregnant women
Culture rather than dipstick
Prescribe an immediate antibiotic, after sending urine for culture, for all pregnant women with symptoms of a UTI
UTI- complicated management
Always send for culture
Longer antibiotic require- 7 days
UTI- catheter management
All catharized patients are bacteriuric
Only send MSU for symptomatic- use narrow range antibiotic according to culture
Change long term catheter before antibiotic use
UTI- catheter symptoms
May be non specific/ atypical for UTI
Fever, flank/suprapubic pain, change in voiding pattern, vomiting, confusion, sepsis
UTI- investigation pyelonephritis
Abd exam- tenderloin, renal angle tenderness, rule out tubal/ ovarian/ appendix pathology
Bloods, USS (to rule out obstruction), MSU
UTI- treatment pyelonephritis
Fluid replace, IV ABx (broad spectrum) for 7-14 days
Catheter
Analgesia
Kidney stones epidemiology
More common in males
Commonest age 30-50 but decreasing
10-15% lifetime risk
Kidney stones location
Anywhere from Collecting duct to External Urethral Meatus
Upper UT- Renal stones, Ureteric stones
Lower UT- Bladder stones, Prostatic stones, Urethral stones
Kidney stones (Calculi)
Consist of crystal aggregates
Deposit anywhere from Collecting duct to External Urethral Meatus
Kidney stones RFs
Anatomical factors
Urinary factors
Infection
Kidney stones RFs- Anatomical factors
Congenital (horseshoe, duplex, PUJO, spina bifida)
Acquired (obstruction, trauma, reflux)
Kidney stones RFs- Urinary factors
Metastable urine, promoters and inhibitors
Calcium, Oxalate, Urate, Cystine
Dehydration
Mechanism of stone formation
“Nucleation theory” suggest that stones form from crystals in supersaturated urine
Types of kidney stones
80% Ca2+ based – oxalate, phosphate
10% uric acid – usually lucent on KUB XR
5-10% struvite – infection stones
1% cystine – congenital
Prevention of kidney stones
Overhydration, low Na diet, healthy Ca/ protein / diary intake
Reduce BMI, active lifestlye
Prevention of kidney stones- uric acid stones
Only form in acid urine
Deacidification of urine to pH7-7.5 preventative
Prevention of kidney stones- cystine stones
Excessive overhydration
Urine alkalinisation
Cysteine binders (eg Captopril, Penicillamine)
+/- genetic counselling
Kidney stones presentation
Asymptomatic or pain (renal colic- lion to groin)
UTI- symptoms/ recurrent
Haematuria, proteinuria, sterile pyuria, anuria
Renal colic pain
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
Investigations for kidney stones
ABC and give analgesia/antiemetic
Urinalysis, MSU if +ve
FBC, U+E, Calcium, Uric acid
Pregnancy test
Imaging- Non contrast CT- KUB scan for any nonpregnant adult patient with suspected renal colic
Uretic colitis- Differential Diagnosis
Kidney stones
Vascular accident – ruptured AAA (>50yo) until proven otherwise
Bowel pathology – diverticulitis, appendicitis
Gynae – ectopic pregnancy, ovarian (cyst) torsion
Testicular torsion
Musculoskeletal
How to interpret NCCT- KUB
1) Count the kidneys
2) Condition of kidneys:
- Perinephric tissues
- Cortical thickness
- Hydronephrosis +/- hydroureter
- Stones
3) Other pathology?
Hydronephrosis
condition where one or both kidneys become stretched and swollen as a result of a build-up of urine inside them
Management of Uretic colic
Analgesia- NSAID suppository/ Opiates
Antiemetic/s
+/- Admit
+/- IV fluids- May make pain worse as diuresis ensues
Observe for SEPSIS
Pyonephrosis
Combination of infection and obstruction, can kill, sometimes very quickly
Can lose renal function in 24 hrs, systemic sepsis leading to septic shock
Management of Uretic colic- Pyonephrosis
-IV Antibiotics. IVI. Oxygen. Escalate
-Drainage- nephrostomy, ureteric stent
Kidney stone- treatment
Depend largely on site and size of stone, patient factors and complications / risks
Options include- conservative, medical, lithotripsy, surgical
Kidney stone- treatment- renal stone: no evidence of obstruction, non-pregnant
1st line hydration + analgesia
Consider antibiotic therapy, watchful waiting
Consider ureteroscopy or ESWL if stone fails to pass after conservative treatment and PCNL for larger stones (>10mm)
Kidney stone- treatment- ureteric stone: no evidence of obstruction, non-pregnant
1st line hydration + analgesia
Consider antibiotic therapy, medical expulsive therapy (alpha-blockers)
Consider ureteroscopy or ESWL if stone fails to pass after conservative treatment and PCNL for larger stones (>10mm)
Kidney stone- treatment- alpha-blockers
Tamsulosin or alfuzosin
Cause ureteric relaxation of smooth muscle and antispasmodic activity of the ureter leading to stone passage
Kidney stone- treatment- ureteroscopy
Tiny wire basket inserted into the lower ureter via the bladder, grabs the stone and pulls the stone free
Kidney stone- treatment- ESWL (Extracorporeal shock wave lithotripsy)
series of shock waves generated by a machine called a lithotripter to break up stones
Can causes problems with fragment passage and clearance
Kidney stone- treatment- PCNL (Percutaneous nephrolithotomy)
Key hole surgery to remove stones when large, multiple or complicated
Kidney stone- treatment- indications for urgent intervention
Presence of infection and obstruction- Pyonephrosis (PCNL/ ureteric stent to remove stone)
Urosepsis, intractable pain or vomiting, impending AKI, bilateral obstructing stones
Kidney stone- treatment- bladder stones
Conservative
Endoscopic- when obstructing
Open / Laparoscopic surgery- ideal for larger stones or if other open procedures required
Gold standard for kidney stone diagnosis
NCCT KUB
Hydronephrosis
Dilation of the renal pelvis or calyces
Obstructive uropathy
functional or anatomic obstruction of urine flow at any level of the urinary tract
Supravesical obstruction
Obstruction above the level of bladder
Infravesical obstruction
Obstruction below the level of bladder
Causes of UT obstructions
Luminal- stones, clots, sloughed papilla, tumours
Mural- congenital or acquired strictures, neuromuscular dysfunction, schistosomiasis- parasitic disease)
Extra-mural- abdominal or pelvic tumour/mass, retroperitoneal fibrosis
Hemodynamic Changes with Unilateral Ureteral Occlusion
Triphasic pattern of renal blood flow and ureteral pressure changes
1-2 hrs after obstruction- RBF + ureteral pressure increase
3-4 hours later- ureteral pressure remain elevated, RBF decreases
5 hrs after obstruction- further decline in RBF and decrease in ureteral pressure
Hemodynamic Changes with Bilateral Ureteral Occlusion
Only a modest increase in RBF lasting 90 minutes followed by a prolonged and profound decrease in RBF (>UUO)
Intrarenal distribution of blood flow changes from the inner to the outer cortex (opposite from UUO)
Hemodynamic Changes with Bilateral Ureteral Occlusion after obstruction is released
Accumulation of vasoactive substances (ANP) cause to preglomerular vasodilation and post glomerular vasoconstriction
When obstruction is released, GFR and RBF remain depressed due to persistent vasoconstriction of the afferent arteriole
Results in post obstructive diuresis
Effects of Obstruction on Tubular Function
Dysregulation of aquaporin water channels in the proximal tubule, thin descending loop, and collecting tubule- polyuria and impaired conc capacity
Na+, K+ and phosphate great excretions during post obstructive diuresis for BUO
UT obstruction investigations
Blood tests – FBC, U&E, Coagulation profile, ABG
Urine – Dipstick / M,C&S
Imaging- Xray, Renal USG, CT Scan
Upper UT obstruction treatment
Nephrostomy or ureteric stent (cause sig discomfort, alpha-blockers need to reduce pain)
Pyeloplasty to widen the PUJ for idiopathic PUJ obstruction
Treat underlying cause if possible
Lower UT obstruction treatment
Ureteral/ suprapubic catheter to relive acute retention
Chronic obstruction only catharize if there is pain, UTI or renal impairment
Treat underlying cause if possible
Nephrotic vs Nephritic syndromes
Nephrotic Syndrome is defined by severe proteinuria, pronounced oedema, and usually normal blood pressure
Nephritic Syndrome showcases haematuria, hypertension, and moderate glomerular damage
Varicocele
Dilated veins of pampiniform plexus- feel like ‘bag of worms’
Left side more commonly effected
May cause dull pain
Varicocele- associations
Subfertility but repair (surgery/ embolization) have little effect on subsequent pregnancy rates
Testicular torsion
Spermatic cord rotates and becomes twisted. The twisting cuts off the testicle’s blood supply and causes sudden pain and swelling
Requires surgery
Testicular torsion- symptoms
Sudden onset pain of one of the testis, which makes walking more uncomfortable
Pain in the abdomen, nausea and vomiting are common
Testicular torsion- signs
Inflammation of one of the testis- vry tender, hot + swollen
Testis may lie high or transversely
Testicular torsion- management
Doppler US may demonstrate lack of BF to testis if unsure
Do not delay on surgery, orchiectomy (full removal) versus orchidopexy (bilateral fixation) is based on the extent of damage to testicular tissue after exposing and untwisting testis
Epididymal cyst
Usually develop in adulthood
Contain clear or milky fluid (spermatocele) fluid, usually lie/above behind the testis
Remove if symptomatic
Hydroceles
Fluid in the tunic vaginalis (investing serosal covering of the testis)
Hydroceles- primary
Associated with a patent processus vaginalis, typically resolves in 1st year of life
More common, larger and usually in younger men
Hydroceles- secondary
Secondary to infection/ tumour/ trauma
Hydroceles- management
Can resolve spontaneously
Aspiration (may be needed) or surgery: plicating the
Acute epididymitis
Inflammation of the epididymis causing pain and swelling that develops over the course of a few days and lasts <6 weeks. It is usually unilateral
Acute epididymitis- common causes in sexually active men
sexually transmitted organisms including Chlamydia trachomatis, Neisseria gonorrhoeae, and Mycoplasma genitalium
Acute epididymitis- common causes in older men
causative organisms are often enteric pathogens, and epididymitis may be associated with bladder outlet obstruction, recent instrumentation of the urinary tract, or systemic illness
Acute epididymitis- diagnostic tests
Gram stain of urethral secretions
Urine specimens for nucleic acid amplification tests for C trachomatis, N gonorrhoeae, and M genitalium
Urine microscopy and culture is also indicated if urinary pathogens are suspected
Acute epididymitis- treatment
Supportive measures- bed rest, scrotal elevation, and analgesics
Empirical antibiotic therapy- antibiotics can be adjusted to target the causative organism
Polycystic kidney disease (PKD)
Inherited renal cystic disease characterised by renal cysts and numerous systemic and extrarenal manifestations
2 types of PKD- dominant (more common) and recessive
Polycystic kidney disease (PKD)- symptoms
Flank/abdominal pain, renal colic, and gross haematuria, and, less commonly, headaches
UTIs occur in 30-50% of pts with PKD
Polycystic kidney disease (PKD)- key diagnostic factors
Renal cysts, hypertension, abdominal/flank pain, haematuria, palpable kidneys/abdominal mass, headaches, dysuria, suprapubic pain, fever
Polycystic kidney disease (PKD)- risk factors
family history of autosomal-dominant PKD (ADPKD) or cerebrovascular event
Polycystic kidney disease (PKD)- investigations
Renal ultrasound usually (CT+MRI can be used for smaller cysts)
Genetic testing for PKD1 or PKD2 although 10-15% of pts have no mutations
Autosomal-dominant Polycystic kidney disease (PKD)- renal ultrasound diagnostic criteria
15 to 39 years of age - at least 3 (unilateral or bilateral) renal cysts;
40 to 59 years of age - at least 2 cysts in each kidney;
>60 years of age - at least 4 cysts in each kidney
Autosomal-dominant Polycystic kidney disease (PKD)- treatment
Renoprotective lifestyle measures
Water intake 3-4L- to supress cyst growth
Hypertensive if HTN
Treat infections with antibiotics
Persistent/ severe pain- may need cyst decompression
