Genitourinary Flashcards
What type of organs are the kidneys? Between which vertebral levels do they lie? What is their blood supply and at which level? What does it contain about a million of?
- Retroperitoneal organs
- Lie between T11-L3
- Blood supply from renal artery direct from aorta at L1
- Contain about a million nephrons
How does urine produced by the kidneys enter the bladder? What type of organ are these?
- Ureters
- Retroperitoneal organs
What anatomical structures make up the lower urinary tract?
Bladder -> bladder neck -> prostate gland -> urethra and urethral sphincter
Give 4 functions of the lower urinary tract.
- Storage of urine
- Converts the continuous process of excretion to an intermittent, controlled and volitional process
- Prevents leakage of stored urine
- Expulsion of urine
Which muscle is involved in contraction of the bladder during micturition? Describe its actions during storage and voiding.
- Destrusor muscle
- Storage = relaxed
- Voiding = contracted
What are the two sphincters in the bladder? How do they differ between male and female? Describe their actions during storage and voiding.
- Internal and external urethral sphincter
- The EXTERNAL urethral sphincter is the same in both males and females
- The INTERNAL urethral sphincter differs - MALES (consists of circular smooth rings, thought to prevent seminal regurgitation during ejaculation). FEMALES (thought to be function, i.e. no sphincteric muscle)
- Storage = urethral sphincters contracted
- Voiding = urethral sphincters relaxed
What type of epithelium lines the bladder?
Urothelium (transitional epithelium)
Describe the nervous control of the bladder and sphincter - which nerves supply the bladder, which vertebral level do they come from, which receptors do they act on and what is their action on the bladder?
- Parasympathetic = make you PEE:
- Pelvic nerves
- S2-4
- Act on M3 receptor
- Make you PEE, i.e. destrusor muscle contraction
- Sympathetic = STORAGE:
- Hypogastric nerves
- T12-L2
- Act on B3 receptor
- STORAGE, i.e. destrusor muscle relaxation
- Somatic:
- Pudendal nerve
- S2-4
- ACh activates nicotinic receptors
- Innervates external urethral sphincter
The bladder is in the storage phase 98% of the time. What are the two reflexes that follow from this?
- Appropriate to void = MICTURITION REFLEX
- Inappropriate to void = GUARDING REFLEX
In the storage phase, why does the pressure remain low as volume increases?
RECEPTIVE RELAXATION, i.e. the bladder expands
Describe the micturition phase.
Higher volumes = bladder expands = afferent impulses stimulate parasympathetic action of detrusor = contraction. Pudendal nerve is inhibited and the external sphincter relaxes
Describe the guarding relfex.
- 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
What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?
Benign prostatic enlargement
What are the lower urinary tract symptoms (LUTS)?
- Storage symptoms:
- Frequency
- Nocturia
- Urgency
- Urgency incontinence
- Voiding symptoms:
- Poor/intermittent stream
- Post-micturition dribbling
- Straining
- Incomplete emptying
- Hesitancy
- HAEMATURIA
- DYSURIA
What might dysuria suggest?
Inflammation
What is benign prostatic hyperplasia? How normal is it?
- Benign prostatic hyperplasia = hyperplasia of the inner transitional zone of prostate gland which partially blocks the urethra
- This is a normal part of ageing for men
What are the complications of benign prostatic hyperplasia?
- Bladder hypertrophy = formation of bladder diverticula
- Urinary retention = bladder calculi
- Residual urine can be infection source = recurrent UTIs
- Hydronephrosis = renal failure
What is the clinical presentation of benign prostatic hyperplasia?
LUTS:
- Storage:
- Frequency
- Urgency
- Nocturia
- Urgency incontinence
- Voiding:
- Poor/intermittent stream
- Post-micturition dribbling
- Straining
- Dysuria
- Incomplete emptying
- Hesitancy
What are the investigations for benign prostatic hyperplasia?
- DIGITAL RECTAL EXAM - shows smooth but enlarged prostate
- PSA - not overly accurate but usually done for completion (remember that you can’t do this at the same time as DRE etc.)
- Urinalysis
- Volume charting
Describe the management of benign prostate hyperplasia.
- 1ST LINE = alpha blockers, e.g. tamsulosin - relaxes smooth muscle in bladder neck and prostate
- 2nd line = 5-alpha reductase inhibitors, e.g. finasteride - blocks conversion of testosterone to dihydrotesterone which decreases prostate size
- If does not respond to medication consider surgery:
- TURP (Transurethral resection of prostate) = GOLD STANDARD. Required if there is acute urinary retention, gross haematuria or spreads to kidneys
- LIFESTYLE - reduce caffeine/alcohol intake, relax when voiding
What is prostate cancer? What is its epidemiology? Which gene mutations is it commonly associated with?
- Prostate cancer = a tumour of glandular origin, situated in the prostate. Most are slow growing but some can be very aggressive and MALIGNANT
- Most common male malignancy and second most common cause of cancer mortality in men in the U.S.A.
- Commonly associated with BRCA1/BRCA2 gene mutations
What are the risk factors for prostate cancer?
- Afro-Caribbean
- Family history/genetics
- Increasing age
- Anabolic steroids
Describe the clinical presentation of prostate cancer. Where does it commonly metastasise to?
- LUTS
- BONE PAIN
- Weight loss
- Fatigue
- Night sweats
- Commonly metastasises to: bone (SCLEROTIC BONY LESIONS), brain, liver, and lung
Describe the investigations for prostate cancer. What is the grading system?
- DRE (cancerous = hard and craggy) and PSA (this is unreliable, with a high rate of false positives/negatives) are done in community
- MULTIPARAMETRIC MRI = 1st line
- TRANSRECTAL USS and BIOPSY = DIAGNOSTIC
- GLEASON GRADING SYSTEM - the higher the score, the worse the prognosism (8-10 is high)
Describe the management for prostate cancer (local and metastatic). How hormone sensitive is it?
- If local: PROSTATECTOMY (<70), ACTIVE SURVEILLANCE (>70 and low risk), RADIOTHERAPY
- If metastatic: CHEMOTHERAPY, RADIOTHERAPY, BILATERAL ORCHIECTOMY (gold standard hormonal treatment), Goserelin (suppresses testosterone production as testosterone stimulates growth of prostate cancer), palliative treatments focusing on relieving symptoms, e.g. TURP
- It is the most hormone sensitive malignancy
What is testicular cancer? Which demographic is it common in? What is the survival rate like? What are the two types of germ cell tumours?
- Testicular cancer arises from the germ cells in the testes. Germ cells are cells that produce gametes (sperm in males). There are other, rare tumours in the testes, e.g. non-germ cell tumours and secondary metastases
- Most common solid tumour in men aged 20-45
- Good survival rate (98% 5 year survival)
- Two types:
- Seminomas
- Non-seminomas (most teratomas)
What are the risk factors for testicular cancer?
- Age 20-45
- Caucasian
- Cryptorchidism
- Previous testicular cancer
- HIV
- Family history
What is the clinical presentation of testicular cancer?
- PALPABLE LUMP WITHIN THE TESTIS - non-transilluminable (light can’t get through tumour), may be painful/painless
- Gynaecomastia (especially Leydig cell tumour)
- Haematospermia
What are the investigations for testicular cancer?
- SCROTAL ULTRASOUND (urgent) is usually the initial investigation
- CXR if symptomatic for pulmonary metastases
- Tumour markers (not always raised, not always diagnostic, can be useful to check response before and after surgery) - alpha-fetoprotein, beta-hCG, LDH
Describe the management for testicular cancer.
Depending on the staging (Royal Marsden used):
- URGENT RADICAL INGUINAL ORCHIECTOMY +/- a testicular prosthesis - this is for seminoma
- CHEMOTHERAPY for non-seminoma (alpha-feto protein)
- Semen cryopreservation
- Treatment for metastatic disease - retroperitoneal lymph node dissection if tumour has metastasised to lymph nodes, chemotherapy, radiotherapy
Where does bladder cancer arise from? What is the most common subtype? What are the most common sites of metastasis?
- Bladder cancer = arises from the urothelium
- Most common subtype is TRANSITIONAL CELL CARCINOMA of the bladder (90%)
- Most common sites of metastasis = lymph nodes, bones, lung, liver
What are the risk factors for bladder cancer?
- Increasing age
- Smoking
- Male
- Caucasian
- Exposure to DYES/RUBBER/LEATHER/TEXTILES + PAINT - hairdresser, painter etc. (so question would be painter and painless visible haematuria)
- Cyclophosphamide (RA/chemotherapy) + previous pelvic radiotherapy
What is the clinical presentation of bladder cancer?
- PAINLESS VISIBLE HAEMATURIA (can be non-visible too, one to remember for exams)
- Urgency
- Suprapubic/pelvic mass pain
- Recurrent UTI
- Symptoms of systemic spread - bone pain, weight loss etc.
What are the investigations for bladder cancer?
- FLEXIBLE CYSTOSCOPY
- Bloods
- Urine sample for microscopy + culture
- Ultrasound
Describe the management for bladder cancer.
- Psychosocial factors: cancer specialist nurse support, Macmillan support
- Medical: radiotherapy, chemotherapy (intravesical therapy or systemic) + symptomatic relief
- Surgical: TRANSURETHRAL RESECTION OF BLADDER TUMOUR (TURBT), radical cystectomy, cystodiathermy
What is the most common type of kidney cancer? How is it usually discovered?
- Most common type is RCC = malignant cancer of proximal convoluted tubule
- Often asymptomatic and discovered incidentally - 25% have metastasis at presentation
What is the clinical presentation of kidney cancer?
Classical triad:
- HAEMATURIA
- Vague LOIN PAIN
- PALPABLE mass in abdomen/lower back
- May present with VARICOCELE - invasion of left renal vein leads to compression of left testicular vein
What are the investigations for kidney cancer?
- USS (1st line)
- CT chest/abdomen/pelvis (more sensitive than USS)
- RENAL BIOPSY = diagnostic
Describe the management for kidney cancer.
Surgery to remove the tumour is first line:
- PARTIAL NEPHRECTOMY = part of the kidney removed
- RADICAL NEPHRECTOMY = entire kidney removed plus surrounding tissue
What are the complications of kidney cancer?
PARANEOPLASTIC CHANGES - polycythaemia, HTN, hypercalcaemia, Cushing’s
What are the 7 functions of the kidney? What is the acronym for this?
- AWETBED:
- Acid-base balance
- Water removal
- EPO
- Toxins
- BP - produces renin
- Electrolyte balance, e.g. sodium, potassium
- Vitamin D activation
(Urea excretion as well)
What is the basic unit of the kidney? In which parts of the kidney are these found?
- Nephron = basic unit of the kidney
- Millions of nephrons in the cortex + medulla:
- Renal corpuscle (glomerulus within Bowman’s capsule) = filter
- Proximal convoluted tubule = for reabsorbing solutes
- Loop of Henle = for concentrating urine
- Distal convoluted tubule = for reabsorbing more water and solutes
- Collecting duct = for reabsorbing water + controlling acid-base + ion balance
What is the cardiac output in L/min? What is the renal blood flow? How about urine flow?
- Cardiac output = 5L/min
- Renal blood flow = 1L/min
- Urine flow = 1ml/min
What is the pathway of the renal artery to the glomerular and peritubular artery?
Renal artery –> interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole –> (nephron) glomerular capillary and peritubular capillary
What is glomerular filtration?
Passage of fluid from the blood into Bowman’s space to form the filtrate
What does the filtration barrier of the glomerulus consist of?
- Endothelium - fenestrated
- Glomerular basement membrane - T4 collagen, -ve charge
- Epithelium - podocytes with foot processes
What can and can’t pass through the filtration barrier?
- Small molecules + ions up to 10kDa can pass freely, e.g. glucose, uric acid, potassium, creatinine
- Larger molecules increasingly restricted
- Fixed negative charge in glomerular basement membrane repels negatively charged anions
What is the glomerular filtration rate (GFR)? How is it calculated? What is the average GFR in a 70kg person?
- The volume of fluid filtered from the glomerulus to the Bowman’s Space per unit time
- GFR = Kf (Pgc - Pbs - Pi gc) - P is hydrostatic pressure, Pi is oncotic pressure
- In a 70kg person the average GFR = 125ml/min
What are the factors affecting GFR?
- Blood pressure = increase in BP –> increased hydrostatic pressure –> increase in GFR
- Size of substance = albumin + all that is attached (lipophilic molecules) to it is unable to cross
- Charge of substance = BM is negatively charged, repels other -vely charged substances, e.g. albumin
- Attachment to protein = albumin
- Capillary permeability
- Surface area
What do we use to measure GFR and why? Which substance do we use clinically? What is the gold standard for measuring inulin?
- Use of a marker substance: free filtered (not attached to large proteins), not metabolised + not secreted/reabsorbed
- Amount excreted per minute = amount filtered per minute
- GFR = Um (concentration of marker substance in urine) x urine flow rate / Pm (concentration of marker substance in plasma)
- Clinically: CREATININE (muscle metabolite)
- GOLD STANDARD = INULIN
Give an example of a marker substance used for estimating GFR.
Creatinine
Estimating GFR: Give 3 essential features of a marker substance.
- Not metabolised
- Freely filtered
- Not reabsorbed/secreted
Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?
Trimethoprim.
Serum creatinine rises and so kidney function (GFR) appears worse
What is the effect on GFR of afferent arteriole vasoconstriction?
Decreased GFR
What is the effect on GFR of efferent arteriole vasoconstriction?
Increased GFR
What is renal clearance? How is this calculated?
- Volume of plasma from which a substance is completely removed by the kidney per unit time
- Marker substance is freely filtered at the glomerulus + is neither reabsorbed nor secreted in the tubule, so all the marker substance that is filtered will end up in the urine, no more (as it is not secreted) and no less (as it is not reabsorbed)
- Clearance = urine concentration x urine volume / plasma concentration
Where in the nephron does the bulk of reabsorption occur?
PCT
What 7 things are reabsorbed at the PCT?
- Sodium
- Chlorine
- Potassium
- Glucose
- Water
- Amino acids
- Bicarbonate
What happens in the loop of Henle? In which nephrons are these found? What are the two cell types lined by?
- 2 parts: descending and ascending
- Descending: H2O reabsorption (impermeable to ions)
- Ascending: Na+, K+ and Cl- reabsorption, has thin (simple squamous epithelium) + thick (low cuboidal) part
- Found only on juxtamedullary (15%) nephrons, cortical (85%) nephrons do not extend into medulla
What happens in the distal convoluted tubule? What is the macula densa?
- Fine tuning, absorption of solutes - beginning to concentrate the urine. Acidified the urine by secreting H+ ions into it
- Exchanges urinary Na+ for body K+, this effect is mediated by aldosterone
- Macula densa = detects Na+ concentration. If low (indicator of low GFR) –> sends signals to release renin –> RAAS –> increase in BP –> increase GFR
What happens in the collecting duct? What are the two cell types and what do they do? What are the cells lined by?
- Acid secretion and concentration of urine, hormones such as aldosterone and ADH act here
- 2 cells:
- Principal cells (respond to aldosterone = exchanging Na+ for K+ and ADH = increasing water reabsorption)
- Intercalated cells (responsible for exchanging acid for base). Alpha intercalated cells secrete acid, beta intercalated cells secrete bicarbonate
What is nephrolithiasis? Who are they more common in? How do they come about?
- Nephrolithiasis = kidney stones. They are hard stones that form in the renal pelvis, where the urine collects before travelling down the ureters
- Slightly more common in men (testosterone -> increased oxolate)
- Stones form when solutes precipitate out as crystals in urine
What are the different types of nephrolithiasis?
- Calcium stones:
- CALCIUM OXOLATE (more common) (80%)
- Calcium phosphate
- Other types of kidney stones include:
- Uric acid – these are not visible on x-ray
- Struvite – produced by bacteria, so associated with infection
- Cystine – associated with cystinuria, an autosomal recessive disease
What are the risk factors for nephrolithiasis?
- Raised serum calcium (hypercalcaemia, hyperparathyroidism)
- Reduced urine output (chronic dehydration, high protein/salt diet)
- Recurrent UTIs
- Congenital abnormalities
What are the two key complications of nephrolithiasis?
- OBSTRUCTION leading to acute kidney injury
- INFECTION with obstructive pyelonephritis
What is the clinical presentation of nephrolithiasis?
- RENAL COLIC. This UNILATERAL LOIN TO GROIN PAIN that can be excruciating (“worse than childbirth”) and COLICKY (fluctuating in severity) as the stone moves and settles
- Restlessness
- N+V
- Haematuria
- Dysuria
What are the investigations for nephrolithiasis? What would these show?
- Urine dipstick usually shows HAEMATURIA
- Bloods: FBC, CRP, U+Es - check for hypercalcaemia and infection
- GOLD STANDARD = NON-CONTRAST CT of the kidneys, ureters and bladder (KUB)
- Abdominal X-ray will show calcium stones but not uric acid stones (radiolucent)
- Ultrasound KUB is less preferred
Describe the management for nephrolithiasis.
- NSAIDs = most effective analgesia, e.g. IM diclofenac
- Antiemetics for N+V, antibiotics if infection
- Watchful waiting for stones <5mm as they usually pass - tamsulosin (alpha-blocker) can help with this
- If do not pass, >10mm, or complete obstruction or infection = SURGERY:
- ESWL (Extracorporeal shock wave lithotripsy) = break stone into smaller fragments using shockwaves
- Uteroscopy
- PCNL (percutaneous nephrolithotomy) = nephroscope inserted to remove stone
- Lifestyle: decrease sodium and protein intake, increased citrus fruit, adequate fluid intake
What is chronic kidney disease? What is the aetiology?
- Abnormal kidney function present for >3 MONTHS
- Aetiology:
- Diabetes
- Hypertension
- Age-related decline
- Glomerulonephritis
- Polycystic kidney disease
- Medications such as NSAIDS, proton pump inhibitors and lithium
What are the risk factors for chronic kidney disease?
- Older age
- Hypertension
- Diabetes
- Smoking
- Use of medications that affect the kidneys, e.g. NSAIDS
Describe the presentation of chronic kidney disease.
- Usually CKD is ASYMPTOMATIC and diagnosed upon testing. Signs and symptoms usually due to uraemia:
- Pruritus
- Nausea
- Reduced appetite
- Oedema
What are the investigations for CKD?
- Bloods: U+E to check the ESTIMATED GLOMERULAR FILTRATION RATE (eGFR):
- G1 = >90 mL/min/1.73m^2
- G2 = 60-89 mL/min/1.73m^2 (<60 = CKD)
- G3a = 45-59 mL/min/1.73m^2
- G3b = 30-44 mL/min/1.73m^2
- G4 = 15-29 mL/min/1.73m^2
- G5 = <15 mL/min/1.73m^2 = end-stage renal failure
- Urinalysis:
- Proteinuria can be checked using urine albumin:creatinine ratio
- Haematuria can be checked using a urine dipstick
- Renal ultrasound
What are the complications of CKD?
- Anaemia
- Renal bone disease
- Cardiovascular disease
- Peripheral neuropathy
- Dialysis related problems
Describe the management for CKD.
- ACE inhibitors are FIRST LINE
- CKD is irreversible in many:
- Slowing the progression of the disease: optimise diabetic control, optimise hypertensive control, treat glomerulonephritis
- Reducing the risk of complications: exercise, maintain a healthy weight and stop smoking, special dietary advice about phosphate, sodium, potassium and water intake, offer atorvastatin 20mg for primary prevention of cardiovascular disease
- Treating complications: ORAL SODIUM BICARBONATE to treat metabolic acidosis, IRON supplementation and EPO to treat anaemia, vitamin D to treat renal bone disease, dialysis in end stage renal failure, renal transplant in end stage renal failure
Who is renal replacement therapy considered for? What are the different types?
- Considered for patients with: END STAGE RENAL FAILURE (eGFR< 15 = stage 5), acidosis not responsive to bicarb, persistent electrolyte disturbances, persistent oedema, severe symptoms of uraemia (seizures, LOC)
- RRT = therapy that replaces the normal blood-filtering function of the kidney:
- Haemodialysis - most common
- Peritoneal dialysis
- Renal transplant
What unit is used to express eGFR?
a) mL/sec/1.73m2
b) mL/min/1.73m2
c) m2/min
d) mL/min
B) mL/min/1.73m^2
What is the most common cause of CKD?
Diabetes
What is acute kidney injury?
Acute kidney injury (AKI) is defined as an acute drop in kidney function. It is diagnosed by measuring the serum CREATININE +/- decreased urine output. Results in IMBALANCE IN ELECTROLYTES and azotaemia (increased creatinine/nitrates) = BAD
What is creatinine?
Creatinine is a waste product made by your muscles as part of everyday activity. Normally, your kidneys filter creatinine from your blood and send it out of the body in your urine. If there is a problem with your kidneys, creatinine can build up in the blood
What are the risk factors for AKI?
- CKD
- Diabetes
- Hypertension
- Older age (> 65 years)
- Nephrotoxic medications, e.g. NSAIDs, ACEi
What are the three types of causes of AKI?
- Pre-renal
- Intra-renal
- Post-renal
Describe the pre-renal causes of AKI.
Pre-renal pathology is the MOST COMMON cause of acute kidney injury. It is due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:
- Dehydration
- Hypotension (shock)
- Heart failure
(decreased volume = decreased perfusion = decreased GFR and decreased creatinine clearance = RAAS activation = increased Na+, urea + BP)
Describe the intra-renal causes of AKI.
This is where INTRINSIC DISEASE in the kidney is leading to reduced filtration of blood. It may be due to:
- Glomerulonephritis - barrier damage + protein leakage = decreased oncotic pressure = decreased GFR
- Interstitial nephritis = inflammation and immune cells =
- Acute tubular necrosis
- Vasculitis
Describe the post-renal causes of AKI.
Post renal acute kidney injury is caused by OBSTRUCTION TO THE OUTFLOW of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an OBSTRUCTIVE UROPATHY. Obstruction may be caused by:
- Kidney stones
- Masses such as cancer in the abdomen or pelvis
- Ureter or urethral strictures
- Enlarged prostate or prostate cancer
What is the clincal presentation of AKI?
- Universal: OLIGURIA (<0.5 mL/kg/hr >6hrs), HIGH CREATININE, hyperkalaemia, uraemia
- Pre-renal: hypotension, signs of liver or heart failure (oedema)
- Intra-renal: infection, signs of underlying disease
- Post-renal: LUTS (BPH)
What are the investigations for AKI?
- URINALYSIS for protein, blood, leucocytes, nitrites and glucose:
- Leucocytes and nitrites suggest infection
- Protein and blood suggest acute nephritis (but can be positive in infection)
- Glucose suggests diabetes
- U+E - eGFR
- CREATININE levels - a rise in serum creatinine of 26 micromol/L or greater within 48 hours
- Ultrasound of the urinary tract is used to look for obstruction
What is the NICE criteria for AKI?
- Rise in creatinine of ≥ 25 micromol/L in 48 hours
- Rise in creatinine of ≥ 50% in 7 days
- Urine output of < 0.5ml/kg/hour for > 6 hours
Describe the management for AKI.
- First step = identify and treat underlying cause:
- FLUID REHYDRATION with IV fluids in pre-renal AKI
- STOP NEPHROTOXIC MEDICATIONS such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
- RELIEVE OBSTRUCTION in a post-renal AKI, e.g. insert a catheter for a patient in retention from an enlarged prostate
Describe the complications of AKI.
- Hyperkalaemia
- Fluid overload, heart failure and pulmonary oedema
- Metabolic acidosis
- Uraemia (high urea) can lead to ENCEPHALOPATHY or PERICARDITIS
Describe 1 pre-renal cause, 1 renal, 1 post-renal cause of AKI.
- Pre-renal: hypotension
- Intra-renal: glomerulonephritis
- Post-renal: kidney stones
List 3 risk factors for AKI.
- CKD
- Hypertension
- Diabetes
Which 2 factors are important for the diagnosis of AKI?
a. Polyuria, serum creatinine
b. Serum creatinine, oliguria
c. Polyuria, eGFR
d. Oliguria, urine creatinine
e. eGFR, serum creatinine
E
What are the different types of urinary tract infections?
- Pyelonephritis - infection of the kidneys
- Urethritis – infection of the urethra
- Cystitis – infection of the bladder
- Prostatitis - infection of the prostate
- Vaginitis – infection of the vagina
What is pyelonephritis? What does it affect? How is it most commonly acquired?
- Pyelonephritis refers to inflammation of the kidney resulting from bacterial infection. The inflammation affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
- Most commonly acquired via ASCENDING TRANSURETHRAL SPREAD but can be via blood or lymphatics
What are the common causes of pyelonephritis?
- Majority are caused by UPEC (gram negative, anaerobic, rod-shaped bacteria)
- Other causes:
- Klebsiella pneumoniae (gram-negative anaerobic rod)
- Enterococcus
- Pseudomonas aeruginosa
- Staphylococcus saprophyticus
- Candida albicans (fungal)
Describe the presentation of pyelonephritis.
- Similar presentation to lower UTIs (i.e. dysuria, suprapubic discomfort and increased frequency) plus the ADDITIONAL TRIAD OF SYMPTOMS:
- Fever, loin pain, N+V
- Patients may also have: systemic illness, loss of appetite, haematuria, renal angle tenderness on examination
Describe the investigations for pyelonephritis.
- 1st line = urine dipstick (will show signs of infection)
- GOLD STANDARD - mid-stream urine for MC+S (microscopy, culture and sensitivity)
- Blood tests will show raised WBCs + raised inflammatory markers, e.g CRP
- Urgent USS to detect stones, obstruction or incomplete bladder emptying
Describe the management for pyelonephritis.
Referall to hospital if there are features of sepsis (SEPSIS SIX (3 tests, 3 treatments):
- Three tests: blood lactate level, blood culture, urine output
- Three treatments: oxygen to maintain oxygen saturations of 94-98% (or 88-92% in COPD), empirical broad-spectrum IV antibiotics (according to local guidelines), IV fluids
What is urethritis? What are the causes?
- Urethral inflammation due to infectious or non-infectious cause
- Infectious: gonococcal (NEISSERIA GONORRHOEA) or non-gonococcal (CHLAMYDIA TRACHOMATIS)
- Non-infectious: trauma, chemical irritation
What are the risk factors for urethritis?
- Biologically male, young
- Multiple sexual partners
- Partner with a sexually transmitted disease (STD)
- Unprotected sexual intercourse
Describe the clinical presentation of urethritis.
- Skin lesion
- Dysuria +/- discharge (blood/ pus)
- Urethral pain
- Penile discomfort/pruritus
What are the investigations for urethritis?
- Nucleic acid amplification tests (NAAT)
- Microscopy and culture of urethral discharge
- Urine dipstick to exclude UTI
- STI testing
Describe the management for urethritis.
Management of underlying cause - antibiotics, e.g. azithromycin and partner notification
What is the major complication of urethritis?
Reactive arthritis - triad of conjuctivitis, urethritis and arthritis - ‘can’t see, can’t pee, can’t climb a tree’
What is cystitis? Who are more susceptible? What are the causes?
- Cystitis is a chronic condition causing inflammation in the bladder
- Women are more susceptible due to SHORTER URETHRA and SHORT PROXIMITY to anus which allows bacteria transfer
- Causes: KEEPS: Klebsiella, E.coli (most common), Enterococci, Proteus species, Staph aureus/saprophyticus
Describe the clinical presentation of cystitis.
- SUPRAPUBIC PAIN, worse with a full bladder and often relieved by emptying the bladder
- FREQUENCY of urination
- URGENCY of urination
- Confusion (in elderly)
- Dysuria
Describe the investigations for cystitis.
- 1st line = urine dipstick = increased leukocytes/blood/nitrates
- Gold standard = MID-STREAM MC+S
- Cystoscopy - for bladder cancer
Describe the management for cystitis.
- Antibiotics: TRIMETHOPRIM/NITROFURANTOIN (3 day course for women, 7 day for men/complicated women). In pregnancy = trimethoprim cannot be used in 1st trimester (inhibits folate synthesis), nitrofurantoin cannot be used in 3rd trimester - amoxicillin, cefalexin can both be used
What is prostatitis? What are the two types?
- Prostatitis refers to inflammation of the prostate. It can be classed as:
- Acute bacterial prostatitis – acute infection in the prostate, presenting with a more rapid onset of symptoms
- Chronic prostatitis – symptoms lasting for at least 3 months
Describe the clinical presentation of acute and chronic prostatitis.
- Chronic prostatitis presents with at least 3 months of: pelvic pain, LUTS, sexual dysfunction, pain with bowel movements + tender and enlarged prostate
- Acute prostatitis = more acute presentation of similar symptoms and systemic symptoms of infection, e.g. fever, myalgia
What are the investigations for prostatitis?
- Urine dipstick testing can confirm evidence of infection
- Urine MC&S can identify the causative organism and the antibiotic sensitivities
- Chlamydia and gonorrhoea NAAT testing on a first pass urine, if sexually transmitted infection is considered
Describe the management of acute and chronic prostatitis.
- Acute:
- Hospital admission for systemically unwell or septic patients
- Oral antibiotics, typically for 2-4 weeks (e.g., ciprofloxacin, ofloxacin or trimethoprim)
- Analgesia (paracetamol or NSAIDs)
- Laxatives for pain during bowel movements
- Chronic:
- Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
- Analgesia (paracetamol or NSAIDs)
- Psychological treatment, where indicated (e.g., cognitive behavioural therapy and / or antidepressants)
- Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
- Laxatives for pain during bowel movements
What is the difference between complicated and uncomplicated UTI?
- Uncomplicated UTI — UTI caused by typical pathogens in people with a normal urinary tract and kidney function, and no predisposing co-morbidities
- Complicated UTI — UTI with an increased likelihood of complications such as persistent infection, treatment failure and recurrent infection
What are the scrotal diseases to study?
- Varicocele
- Testicular torsion
- Epididymal cyst
- Epididymitis
- Hydrocele
What is a varicocele? Which side is more affected and why?
- A varicocele is the abnormal dilation of the internal spermatic veins and pampiniform plexus that drain blood from the testis
- Left side more commonly affected (angle that left testicular vein enters the left renal vein = increased flow resistance)
What is varicocele the most common cause of in young adults?
Scrotal enlargement
What are the complications of varicocele?
Testicular damage = atrophy = poor sperm production + quality = infertility
What is the clinical presentation of varicocele?
- Feels like a BAG OF WORMS
- Dragging/soreness/heaviness of the scrotum
What are the investigations for a varicocele?
- Clinical diagnosis
- Doppler ultrasound
- Semen analysis
Describe the treatment for varicocele.
Surgical repair if there is pain, infertility, or testicular atrophy
What is testicular torsion? What does a delay in treatment cause?
- Testicular torsion refers to twisting of the spermatic cord with rotation of the testicle
- It is a urological emergency - delay in treatment increases the risk of ischaemia and necrosis of the testicle, leading to sub-fertility or infertility
Describe a cause of testicular torsion.
- A BELL-CLAPPER DEFORMITY is one of the causes of testicular torsion
Normally, the testicle is fixed posteriorly to the tunica vaginalis. A bell-clapper deformity is where the fixation between the testicle and the tunica vaginalis is absent. The testicle hangs in a horizontal position (like a bell-clapper) instead of the typical more vertical position. It is also able to rotate within the tunica vaginalis, twisting at the spermatic cord. As it rotates, it twists the vessels and cuts off the blood supply
What is the clinical presentation of testicular torsion?
- Sudden onset of acute, severe pain
- Firm swollen testicle (on examination)
- Elevated (retracted) testicle (on examination)
- Absent cremasteric reflex (on examination)
- Abnormal testicular lie - often horizontal (on examination)
What are the investigations for testicular torsion?
UNNECESSARY IF CLINICAL FINDINGS ARE STRONGLY SUGGESTIVE:
- Colour Doppler ultrasound - absent of decreased blood flow in affected testicle. Can show a whirlpool sign (spiral appearance to spermatic cord and blood vessels)
Describe the treatment for testicular torsion.
- SURGICAL DETORSION within 6 hours
- Orchiopexy (correcting the position of the testicles and fixing them in place)
- Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis
What is an epididymal cyst? What does it contain? Are they confined to one testis? What is the treatment?
- Smooth extra testicular spherical cyst at the epididymis (top of the testicle)
- Contains clear and milky fluid - TRANSLUMINATES (fluid-filled)
- May be multiple and bilateral. When they get large can be painful. Can palpate the cyst and testis separately
- No treatment is usually necessary
What is epididymitis? What are the causes?
- Inflammation of the epididymis
- Causes:
- Infectious, e.g. E.coli, Chlamydia trachomatis
- Non-infectious, e.g. trauma, autoimmune disease
What is the clinical presentation of epididymitis?
- Usually unilateral scrotal pain, sometimes radiates to abdomen with/without swelling
- Fever, chills
- LUTS
Describe the investigations for epididymitis.
- Gram stain of urethral secretions
- Urine dipstick test, microscopy, and culture
- Colour Doppler ultrasound - enlarged, thickened epididymis with increased blood flow = excludes testicular torsion
Describe the treatment for epididymitis.
- Infectious epididymitis: ceftriaxone, doxycycline
- Non-infectious: treat underlying cause
What is a hydrocele? What are the two types?
- A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes:
- Simple hydrocele: processus vaginalis is closed and more fluid is being produced by the tunica vaginalis (fluid trapped in the tunica vaginalis) than is being absorbed
- Communicating hydrocele: the tunica vaginalis is connected with the peritoneal cavity via the processus vaginalis. This allows fluid to travel from the peritoneal cavity into the hydrocele, allowing the hydrocele to fluctuate in size
In hydrocele, what is found upon examination of the testes?
- Non-tender smooth cystic swelling
- Painless unless infected
- TRANSILLUMINATES with light
What are the key differential diagnoses of a scrotal or inguinal swelling in a neonate?
- Hydrocele
- Partially descended testes
- Inguinal hernia
- Testicular torsion
- Haematoma
- Tumours (rare)
What is a useful investigation for hydrocele?
After clinical diagnosis, ULTRASOUND is useful for confirmation of diagnosis and excluding other causes
Describe the management for simple and communicating hydrocele.
- Simple hydroceles = usually resolve within 2 years without having any lasting negative effects. They may require surgery if they are associated with other problems, such as a hernia
- Communicating hydroceles = can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele (the processus vaginalis)