Genitourinary Flashcards
Renal colic (nephrolithiasis) definition
Nephrolithiasis refers to the presence of crystalline stones (calculi) within the urinary system (kidneys and ureter). Such renal stones are composed of varying amounts of crystalloid and organic matrix. Ureteric stones almost always originate in the kidney but then pass down into the ureter. Most common cause of urinary obstruction.
Composition of stones:
- calcium stones (80%) - calcium oxalate (80% of Ca stones) - oxalate rich foods eg spinach, chocolate; calcium phosphate (20% of Ca stones)
- uric acid stones (10-20%) - gout is a risk factor
- cystine stones (1%) - genetic conditions
- struvite stones (1-5%) - caused by infection, proteus, Pseudomonas & Klebsiella (not e. coli)
Renal colic (nephrolithiasis) aetiology
Usually due to elevated levels of urinary solute such as calcium, oxalate, uric acid and sodium as well as decreased levels of stone inhibitors such as citrate and magnesium
Renal colic (nephrolithiasis) risk factors
Dehydration, high salt intake, white, male, obesity
Renal colic (nephrolithiasis) pathophysiology
Presence of stones (calculi) within the urinary system.
Usually symptom free but cause renal calico when stuck.
3 common sites stones get:
- pelvic-ureteric junction (PUJ)
- pelvic brim
- vesicle-ureteric junction
Renal colic (nephrolithiasis) key presentations
Classical renal coli is described as severe, acute flank pain that radiates to the ipsilateral groin ‘Loin to groin’.
Pain is mostly constant
Renal colic (nephrolithiasis) signs and symptoms
Nausea and vomiting, urinary frequency/urgency, dysuria (painful urination), testicular pain, rigours (shaking) and fever may be present with pyelonephritis as a complication.
Renal colic (nephrolithiasis) 1st line investigations
Urine dipstick - haematuria
Midstream specidium urine (MSU)
Bloods: FBC, CRP & ESR, renal function (creatinine) & calcium
KUB X-ray
Renal colic (nephrolithiasis) gold standard investigations
NCCT KUB (non-contrast computerised tomography of the Kidneys Ureter Bladder) - 99% sensitive and diagnostic
Renal colic (nephrolithiasis) differential diagnosis
Ruptured AAA if >50 years until proven otherwise
Renal colic (nephrolithiasis) management
Watchful waiting and strong analgesic - IV diclofenac
Antibiotics - IV cefuroxime/gentamicin
Medical expulsive therapy (MET) - PO nifedipine/alpha blocker eg tamsulosin
Lithotripsy
Percutaneous nephrolithotomy
Renal colic (nephrolithiasis) monitoring
Prevention:
Non medical: adequate hydration, reduce sodium, fat and protein, reduce oxalate rich food
Medical:
- hypercalciuria and recurrent calcium stones: thiazide diuretic
- uric acid stones: allopurinol
- cystine stones: captopril
Acute kidney injury/acute renal failure definition
Acute Kidney Injury (AKI), previously called acute renal failure is an acute decline in kidney function leading to a rise in serum creatinine and/or a fall in urine output. The disease is a spectrum from mild kidney injury to severe kidney failure
Acute kidney injury/acute renal failure aetiology
AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease.
Pre-renal: low renal perfusion/obstruction of flow
- volume depletion: haemorrhage, diarrhoea, dehydration
- hypotension: hypovolemia, sepsis
- cardiovascular
- atherosclerosis/ischaemia
Intrarenal: renal parenchyma (function tissue) damage
- glomerulonephritis: nephritic and nephrotic syndromes
- acute tubular necrosis: nephrotoxins: ACEi, NSAIDs, amino glycoside abx eg gentamicin
- vascular disease: vasculitis, HTN
Post-renal: outflow obstruction
- benign prostatic hyperplasia
- kidney stones
- tumour
- retroperitoneal fibrosis
Acute kidney injury/acute renal failure risk factors
Sepsis, age >75yrs, DM, cardiac failure, drugs, increased fluid loss or decreased fluid intake
Acute kidney injury/acute renal failure pathophysiology
Rapid reduction in kidney function: hours-days
Decline in GFR = loss of normal/water/solute/acid-base homeostasis
Causes retention of ammonia and uric acid and dysregulation of extracellular volume and electrolytes
Pre-renal: the kidney responds to lower perfusion pressure by enhancing sodium and water reabsorption. Baroreceptors in the carotid artery and aortic arch respond to lower blood pressure with sympathetic stimulation. This, along with vasoconstriction of the glomerular efferent arteriole and dilation of the afferent arteriole is intended to maintain glomerular filtration. Decreased perfusion promotes in the RAAS. Aldosterone release promotes further water and sodium reabsorption at the collecting duct. Low blood volume also stimulates the hypothalamus to release ADH to increase tubular water re-absorption and therefore concentrates the urine.
Post-renal: kidney injury from obstruction results from increased intratubular pressure yielding tubular ischaemia and atrophy. There may also be an influx of monocytes and macrophages. Cytokines, free radicals, proteases and TNF-b are released causing irreversible tubular injury and fibrosis when obstruction becomes chronic.
3 criteria are used to diagnosis AKI, any 1 of these = Dx of AKI
- rise in serum creatinine >0.3mg/dL in 48hrs
- rise in creatinine >50% baseline within 7 days
- urine output <0.5ml/kg/hr for >6 consecutive hrs
Acute kidney injury/acute renal failure key presentations
Hypotension, presence of risk factors (patients are very often asymptomatic),
History of kidney insults, reduced urine production (commonly oliguria, anuria suggests obstructive cause or severe AKI from pre-kidney or intrinsic cause),
Lower urinary tract symptoms such as urgency, frequency or hesitancy are suggestive of urinary tract obstruction
Dizziness and postural hypotension are consistent with hypovolaemia and suggest pre-kidney AKI (may also have thirst)
Fluid overload (increased JVP, peripheral oedema, HTN)
Systemic: nausea, vomiting, confusion
Very early stages - often asymptomatic
May have oliguria or anuria
Biochemical abnormalities
- hyperkalemia - arrhythmias, muscle weakness etc
- hyponatremia - headaches, nausea, poor balance etc
- metabolic acidosis
- hyperphosphatemia
Uraemia - weakness, fatigue, anorexia, nausea, vomiting
- can cause seizures, coma, uraemia pericarditis if untreated
Acute kidney injury/acute renal failure investigations
Bloods: FBC, U&E + creatinine kinase, CRP, immunology
Urinalysis - urine dipstick and urine osmolality
ABG
Establishing cause:
- blood urea nitrogen (BUN): creatinine ratio
- urine osmolality
- urine sodium excretion
- fractional excretion of sodium
Acute kidney injury/acute renal failure management
Best treatment is prevention (monitor urinary output and creatinine levels)
Manage fluid balance, hyperkalemia, acidosis
Manage cause:
- pre-renal: fluids, circulatory/cardiac support, treat underlying sepsis
- intrarenal: specialist treatment, kidney biopsy etc
- post renal: catheter, nephrostomy, urological intervention
If severe - harm-dialysis, peritoneal dialysis or hemofiltration
Cancer - kidney definition
Cancers that start in the kidney. Transitional cell carcinomas can also occur in renal pelvis, calyx, ureter and urethra
Cancer - kidney aetiology
Renal cell carcinomas are the most common (80%)
- adenocarcinoma - proximal tubule epithelium
- highly vascular
- metastasis - bone, liver, lungs
Risk factors: smoking, HTN, CKD, PKD, haemodialysis
Nephroblastoma (Wilms Tumour): childhood tumour (>3yrs) - from primitive renal tubules and mesenchymal cells
Cancer - kidney signs and symptoms
Signs: abdo mass, haematuria, obstruction
Symptoms: loin pain, general cancer symptoms
Nephroblastoma: suspect if abdominal mass and haematuria in children
Cancer - kidney diagnosis
Bloods: polycythemia (increased EPO secretion), U&Es, Ca++ (high Ca is poor prognostic marker)
Urine: check for haematuria
CT/MRI: staging
USS: visualise tumour
Cancer - kidney management
Radical nephrectomy - if localised Metastatic/non-resectable - mTOR inhibitors (temsiolimus) - TKI (sunitinib, sorafenib) - monoclonal antibodies (bevacizumab) RCC can be very chemo/radio resistant
Cancer - bladder definition
Cancers of the bladder
Cancer - bladder aetiology
3 main types: - transitional cell carcinoma - squamous cell carcinoma - adenocarcinoma Risk factors: rubber, azo dyes, schistosomiasis (squamous types), chronic cystitis, smoking, male > female
Cancer - bladder presentations
Painess haematuria
Presence of risk factors
Dysuria
Cancer - bladder diagnosis
Urinalysis: haematuria is typical, pyuria (WCCs in urine) may be present
Cystoscopy
Biopsy
CT urogram
Involved lymph nodes often para-aortic iliac
Cancer - bladder management
T1: surveillance, resection of bladder tumour, cystoscopy and diathermy, chemo
T2-3: radical cystectomy, chemo
T4: palliative chemo/radio
Cancer - bladder complications
Prostatic urothelial carcinoma or other urinary tract TCC
Cancer - prostate definition
Malignant tumour situated in the prostate gland
Cancer - prostate aetiology
Malignant adenocarcinoma. High-fat diet, high testosterone levels and genetics are thought to increase the risk
Cancer - prostate presentation
Lower urinary tract symptoms (nocturne, dysuria etc) although they are generally a sign of higher - T - stage or benign prostatic hyperplasia.
Abnormal digital rectal examination.
General cancer symptoms and bone pains may be present
Cancer - prostate diagnosis
DRE: hard and irregular PSA (prostate specific antigen): PSA can be raised due to prostatic and benign prostatic hyperplasia, raised TRUS Biopsy Imaging Bone scan
Cancer - prostate management
Localised (low risk) - surveillance
Disease progressing/advance - radical treatment
- radical prostatectomy
- radical radiotherapy
Hormone therapy: LHRH agonists + anti-androgen
Chemo and surgery may be needed
T staging:
1: non playable
2: palpable and confined to prostate
3: palpable and through capsule
4: palpable and invade other structures
Cancer - prostate complications
Metastasis to adjacent structures, bone and lung
Cancer - testicular definition
The most common malignancy in young adult men and highly curable if diagnosed early
Cancer - testicular aetiology
Most common type is germ cell tumours - seminomas - nonseminomas Sex cord (stromal) Mixed Lymphoma
Risk factors: undescended testes, infant hernia, infertility
Cancer - testicular presentation
Painless testicular lump
Presence of risk factors, young male
May have a secondary hydrocele
Metastatic symptoms
- cough and dyspnoea - lung
- abdominal mass - enlarged lymph nodes
- back pain - para-aortic lymph nodes
- left testicular cancer can spread to left kidney
Cancer - testicular diagnosis
Scrotal US Biopsy Serum tumour markers - A-fetoprotein - B-hCG (never found in normal men) - lactate dehydrogenase, LDH
Staging
- No mets
- Para-aortic - infradiapharhmatic
- Supradiaphrahmatic
- In lungs
Cancer - testicular management
Seminomas - radical orchiectomy (removal of testicle) and radiotherapy
Non-seminomas - chemo
Cancer - testicular complications
Metastasis
Chronic kidney disease definition
Kidney damage (proteinuria, haematuria or anatomical abnormality) present for >3 months and/or impaired GFR. Normal GF: 100-120ml/min/1.73m^2
GI: normal or high; >=90
G2: mildly decreased; 60-90
G3a: mildly to moderately decreased; 45-59
G3b: moderately to severely decreased; 30-44
G4: severely decreased; 15-29
G5: kidney failure; <15
Chronic kidney disease aetiology
Prerenal:
- heart failure
- cirrhosis
Intrarenal:
- hypertension
- diabetes
- renal artery stenosis
- systemic disease: SLE, RA
- glomerular disease
- long use of NSAIDs
- nephrotoxic substances (lead, tobacco)
Postrenal:
- benign prostatic hyperplasia
- repeated pyelonephritis
Chronic kidney disease clinical manifestations
- protinuria
- haematuria
- oedema
- polyuria, nocturne, oliguria
- uraemia
- general: lethargy, pruritus, cramps etc
- anaemia
Chronic kidney disease investigations
FBC, U&Es, vitamin D TFTs (PTH) Bloods for serum creatinine and estimated glomerular filtration rate (eGFR) Urine sample (albumin:creatinine ratio) Urine dipstick (check for haematuria) Ultrasonography
Chronic kidney disease monitoring
eGFR and urine ACR tests are repeated within 3 months to confirm diagnosis
Chronic kidney disease complications
Cardiac arrhythmias (hyperkalaemia)
Hypertension (increased renin secretion)
Anaemia (decreased EPO)
Renal osteodystrophy
- hypocalcaemia, hyperphosphatemia
- secondary hyperparathyroidism
- skeletal abnormalities, arterial calcification
In end-stage renal disease: azotaemia (abnormally high nitrogen)
- uremic encephalopathy and polyneuropathy
- ureic pericarditis
- ureic frost
Benign prostatic hyperplasia (BPH) definition
Lower urinary tract symptoms (LUTS) caused by bladder outlet obstruction due to benign prostatic hyperplasia
Benign prostatic hyperplasia (BPH) aetiology
Hyperplasia of the epithelial and stromal compartments occur particularly in the transitional zone. Age and hormonal changes likely have an effect
Benign prostatic hyperplasia (BPH) risk factors
Age >50yrs, family history, non-Asian race, cigarette smoking
Benign prostatic hyperplasia (BPH) pathophysiology
Dihydrotestosterone may be linked to the development
Benign prostatic hyperplasia (BPH) clinical manifestations
LUTS symptoms: Voiding - hesitancy - poor stream - urinary retention - terminal dribbling - overflow incontinence
Storage
- frequency
- urgency
- nocturia
Benign prostatic hyperplasia (BPH) investigations
DRE - smooth and enlarged
PSA - rule out cancer or prostatitis
TRUS
Benign prostatic hyperplasia (BPH) management
Lifestyle - avoiding caffeine and alcohol
Medical
- 1st line: a-blockers (reduce smooth muscle tone)
- 2nd line: 5a-reductase inhibitors
Surgery
Catheterisation
Urinary Tract Infection - pyelonephritis (acute/chronic), cystitis definition
A UTI is the presence of characteristic symptoms and significant bacteriuria in the urinary tract
Lower UTI: cystitis (bladder infection)
Upper UTI: pyelonephritis (kidney infection)
Urinary tract infection epidemiology
Very common clinical problem, second most common reason for antibiotic prescription. Much more common in women
Urinary tract infection aetiology
E. coli - majority (80-85%) KEEPS - common aetiologies - Klebsiella - E. coli - Enterococci - Proteus - Staphylococcus (usually coagulase negative)
Urinary tract infection risk factors
Sexual activity, new sexual partner, diabetes (bacteria grow faster in sugary urine), old age, presence of catheter, pregnancy
Urinary tract infection clinical manifestations
Urinary frequency
- painful, frequent and in small amounts
Dysuria (painful or difficult urination)
Foul-smelling cloudy urine (pyuria), urgency, suprapubic/loin pain, rigors and fever (suggests pyelonephritis)
Haematuria may be present
Acute confusion (especially in elderly)
Urinary tract infection 1st line investigations
Urine dipstick - leukocytes and nitrate suggest UTI
Urinary tract infection gold standard investigations
MSU
- microscopy for leukocytes
- culture and sensitivity for Abx choice
Urinary tract infection differential diagnosis
Pyelonephritis is more associated with fever, nausea and vomiting. Flank tenderness is common on examination. Costovertebral angle tenderness is a common finding
Urinary tract infection management
1st line (cystitis): trimethoprim 1st line (pyelonephritis): ciprofloxacin 1st line (if pregnant): nitrofurantoin
Prostatitis definition
Inflammation within the prostate that is usually accompanied by evidence of recent or ongoing infection. Most frequent urological diagnosis in men < 50yrs
Prostatitis aetiology
E. coli is the main cause (80%)
Eneterococcus is the next most common
Pseudomonas, proteus mirabilis, Klebsiella can also be the cause
Prostatitis presentation
Hallmark is acute onset of lower urinary tract symptoms (dysuria, urinary frequency, perineal discomfort) accompanied by systemic signs (fever, chills, malaise)
Prostatitis diagnosis
Digital Rectal exam shows an intensely tender prostate
Urinalysis: leukocytes, bacteria (follow up with culture)
Prostatitis management
Ciprofloxacin + NSAID
May be surgical relief if obstruction present
Prostatitis complications
Urinary retention, sepsis
Urethritis definition
Inflammation of the urethra. Common and treatable bacterial condition
Urethritis aetiology
Causes divided by gonococcal (GU) or non-gonococcal. Most important are Neisseria Gonorrhoeae and Chlamydia trachomatis
Urethritis presentation
Often occurs in people with new or multiple sex partners, inconsistent use of condoms
Urethral discharge - primary symptom, usual onset is between 4 days and 2 weeks after contact
Urethral irritation or itching
Dysuria
Orchialgia - sensation of heaviness in male genitals - pain suggests epididymitis or orchitis
Urethritis diagnosis
Gram stain of urethral discharge - gram negative diplococci is suggestive of gonorrhoea
Nucleic acid amplification tests - most sensitive for gonorrhoea detection from urine
Culture of discharge - chocolate agar positive for Neisseria gonorrhoea, HIV test - standard to rule out
Urethritis management
1st line (gonococcal): ceftriaxone and azithromycin 1st line (non-gonococcal): azithromycin
Glomerular disease - nephritic syndrome definition
Characterised by thinning of the glomerular double basement membrane and porous podocytes as well as inflammation. When it occurs in the glomerulus it is called glomerulonephritis (inflammation within the kidney/renal vessels resulting in glomerular damage and its function).
Glomerular disease - nephritic syndrome aetiology
Children: IgA nephropathy - 1-2 days after upper respiratory tract infection (URTI) Post-streptococcal glomerulonephritis - 2-3weeks after URTI due to strep Henoch-Schonlein Purpur (HSP) - palpable purpura, abdo pain, joint pains and renal damage Haemolytic-uraemic syndrome - after E. coli infection
Secondary (most common in adults):
Goodpasture’s syndrome (autoimmune)
Other autoimmune eg SLE
Vasculitides
Glomerular disease - nephritic syndrome pathophysiology
The pores of the podocytes become large enough to allow RBCs and proteins to pass through. The capillaries of the glomerulus swell causing increased renin secretion due to extra stretch on the juxtaglomerular apparatus and eventually leading to hypertension
Glomerular disease - nephritic syndrome key presentations
- haematuria
- proteinuria (<3.5g/day)
- hypertension
- oedema (less than nephrotic)
Glomerular disease - nephritic syndrome investigations
History and exam: signs of fluid overload eg oedema, raised JVP, HTN, history of URTI in child suggests IgA/post-strep
Bloods: electrolytes, creatinine (for GFR), ANA antibody screen, anti-GM antibody (Goodpasture’s), ANCA
Urinalysis
Glomerular disease - nephritic syndrome management
Fluid restrictions to reduce oedema - also reduce kidney workload
Diuretics if fluid overload is severe
Antihypertensives to normalised BP
NSAIDs or steroids - reduce active inflammation in the kidney
Glomerular disease - nephrotic syndrome definition
Nephrotic syndrome is defined as proteinuria (>3.5g/24hrs), hpoalbuminemia (<30g/L), oedema and NO BLOOD. Lipiduria and hyperlipidemia are less common and less important
Glomerular disease - nephrotic syndrome aetiology
Primary:
- minimal change disease - so called because nephrons appear normal under a light microscope. This is the most common in children
- focal segmental glomerulosclerosis - most common in young adults
- membranous glomerulonephritis - most common in adults
Secondary:
- infection eg HIV, Hep B
- autoimmune eg SLE, RA, vasculitides
- diabetes mellitus
- neoplasms eg myeloma, leukaemia
- drugs eg NSAIDs
Glomerular disease - nephrotic syndrome pathophysiology
Proteins lost are mostly albumins resulting in hypoalbuminemia causing oedema seen because of lower osmotic pressure within vessels causes fluid to accumulate in interstitial tissue fluid
Glomerular disease - nephrotic syndrome clinical manifestations
Oedema
- especially facial swelling in children
- peripheral (ankle and legs) in adults
Frothy urine - due to lipids and proteins in urine Tiredness Breathness - pearl effusion may occur due to severe hypoalbuminemia AKI
Glomerular disease - nephrotic syndrome investigations
1st line: urine dipstick - proteinuria and NO HAEMATURIA
MSU (midstream specimen of urine) - microscopy, culture and sensitivity for UTI
Gold standard: protein:creatinine or albumin:creatinine ratio
Renal biopsy for aetiology
Bloods: ESR CRP (for SLE/autoimmune), FBC, LFTs
CXR for plural effusion if suspected
Glomerular disease - nephrotic syndrome management
Sodium and fluid restriction and high dose diuretic - reduces oedema - furosemide Coticosteroids - reduces kidney damage and proteinuria - prednisolone
Medical nutrition therapy for lost protein
Glomerular disease - nephrotic syndrome complications
Thromboembolism, infection, hyperlipidaemia
Polycystic kidney disease - dominant and recessive definition
PKD is part of a group of disorders characterised by renal cysts and numerous systemic and extra-renal manifestations. Can be divided into autosomal-dominant PKD (ADPKD) and autosomal-recessive PKD (ARPKD), the former of which being much more common.
Chromosome 16.
Polycystic kidney disease aetiology
ADPKD:
- mutation in the PKD1 gene (codes for polycystic 1) - makes up for approx 85% of cases
- mutation in the PKD2 gene (codes for polycistin 2)
ARPKD: mutation in PKHD1 gene, which codes for fibrocystin, a protein which is involved with polycystic 2’s function
Polycystic kidney disease risk factors
Family history of PKD, or cerebrovascular event or berry aneurysms (subarachnoid haemorrhages)
Polycystic kidney disease pathophysiology
Polycystins are protein channels found in the cell membrane of ciliated cells in the nephrons and throughout the body - these channels are involved in inhibition of cell division, so they absence results in uncontrolled division resulting in cysts throughout the body (particularly the kidneys)
Renal cysts cause compression of normal renal architecture and intrarenal vasculature, increased renal size, interstitial fibrosis and tubular atrophy and progressive renal impairment.
Polycystic kidney disease key presentations
Family history of PKD or end stage renal disease (ESRD)
Polycystic kidney disease signs and symptoms
- renal cysts
- excessive water and salt loss
- nocturne
- hypertension (often at a young age)
- abdominal/flank pain (due to nephrolithiasis or UTIs etc)
- haematuria
- palpable kidneys (bilateral kidney enlargement)
- UTI symptoms common
- cholestasis due to aneurysms in bile ducts
- berry aneurysms, particularly in the circle of willis (leading to subarachnoid haemorrhages)
- cardiac murmur: mitral valve prolapse, mitral regurgitation. aortic regurgitation and dilated aortic root are the most common
- abdominal hernias are common
- portal HTN
- hepatomegaly - highly specific for ADPKD
Polycystic kidney disease 1st line investigations
Renal ultrasound
- at least 2 unilateral or bilateral cysts < 30 yrs
- at least 2 cysts in each kidney 30-59yrs
- at least 4 cysts in each kidney >60yrs
CT scan: better sensitivity
Urinalysis: assess albumin excretion, creatinine often normal
Scrotal disease definition
Epididymal cyst: cyst of the epididymis containing clear serous liquid. Above and behind the testes. Most common around 40 yrs, rare in children. A spermatocele is a cyst in the head of the epididymis.
Hydrocele: accumulation of clear fluid within the cavum vaginale (between the layers of the tunica vaginalis)
Varicocele: enlargement of the pampiniform plexus in the scrotum
Hematoceles: collection of blood in the tunica vaginalis around the testes
Epididymitis (also known as epididymo-orchitis): inflammation of the epididymis, epididymo-orchitis is when there is also orchitis (inflammation of testis)
Testicular torsion: twisted spermatic cord - cut off blood supply to the testes -ischaemia - this is a medical emergency
Scrotal disease aetiology
Epididymal cyst/Spermatocele: clear/milk fluid above and behind testes
Hydrocele: trauma/infection/tumour
Varicocele: likely combination of anatomical factors
Hematoceles: trauma
Epididymitis: among sexually active men, Chalmydia trachoma’s and Neisseria gonorrhoeae are the most common cause. May be due to Escherichia coli and Proteus
Scrotal disease presentation
Epididymal cyst: soft squidgy lump at top or bottom of the testicle. Can get above it and separate from testis. Can transilluminate (light can be shone through)
Hydrocele: scrotal enlargement, smooth swelling, no pain normally, can usually get above it. Testis not palpable separately. Cystic so not solid mass. Can transilluminate.
Epididymitis: unilateral scrotal pain and swelling of gradual onset, tenderness, hot, diffuse enlargement of the testis. May have urethritis and discharge, sweats and fevers. Can get above it, epididimytis is separate, orchitis is testicular. Solid - feels like mass. Does not transilluminate.
Testicular torsion: sudden onset testicular pain, inflamed and tender testicle, unilateral, abdo pain, N&V.
Scrotal disease diagnosis
Epididymal cyst: usually clinical may need USS
Hydrocele: clinical diagnosis, may need USS
Varicocele: clinical diagnosis, may need doppler ultrasound
Epididymitis: gram stain of urethral secretions, urine dipstick (leukocytes), urine microscopy and cultures, nucleic acid amplification test (NAAT)
Testicular torsion: clinical
Scrotal disease differential diagnosis
Assume a testicular lump is cancer until proven otherwise
Scrotal disease management
Epididymal cyst: generally harmless and don’t require treatment, may need surgery if painful
Hydrocele: observation, may need surgery/aspiration of discomfort or infection
Varicocele: reassurance, observation. Venography, doppler ultrasound, surgery if needed
Hematoceles: aspirate/surgery
Epididymitis: abx, ceftriaxone and doxycycline
Testicular torsion: fast referral to urology for surgery
Obstructive uropathy definition
The blockage of urinary flow can affect one or both kidneys. If only one is affected urinary output may be unchanged and serum creatinine can be normal. When kidney function is affected it is called obstructive nephropathy
Obstructive uropathy aetiology
Unilateral obstructive uropathy: acute unilateral uropathy is most commonly due to renal stones. It may be from injury during surgery. Chronic unilateral uropathy may be due to malignancy in nearby structures
Bilateral obstructive uropathy: benign prostatic hyperplasia (BPH) is a common cause and can cause acute or chronic uropathy.
Back pressure on the kidneys leads to decreased renal blood flow, decreased GFR, and up-regulation go the RAAS. This can lead to atrophy and apoptosis on the renal tubules.
Obstructive uropathy presentation
Flank pain: especially if unilateral
Fever: sign of UTI
LUTS: frequency, urgency, incomplete emptying etc
Palpable bladder
Costovertebral angle tenderness: common with obstruction and infection
May have signs of sepsis: tachypnea, tachycardia, hypotension, altered mental state
Obstructive uropathy diagnosis
Urinary dipstick: nitrates and blood or leukocyte esterase indicates UTI
Renal ultrasound: may show hydronephrosis
For stones: CT pyelogram, intravenous pyelogram
Obstructive uropathy management
If due to calculi (stones)
- analgesia (ketorolac), rehydration and alpha blockers tamsulosin
- may need active stone removal
May need ureteric stent or catheterisation, abx if infection suspected (treat as UTI)
Urinary incontinence definition
Loss of control of voiding in the bladder. More common in women
Neuropathic Bladder Dysfunction: spinal/CNS injury or disease - loss of neuronal control over bladder
- spastic injury: higher spinal cord - hyperreflexcic - bladder is functional but not controlled by brain - loss of coordination and completion of voiding - involuntary urination - urger incontinence
- flaccid injury: lower spinal cord - hyporeflexic - bladder is areflexic - bladder fills until it overflows - stress incontinence - consider permanent catheterisation
Urinary incontinence aetiology
Urge incontinence: due to detrusor overactivity and bladder hypersensitivity.
Stress incontinence: due to sphincter and pelvic floor weakness. Women - secondary to birth trauma. men - post-prostatectomy
Overflow incontinence: usually a sensation of incomplete emptying after voiding. Diabetic neuropathy can impairment ability of detrusor to contract
Urinary incontinence management
Oxybutynin for urge incontinence - anticholinergic
AKI complications
Pulmonary oedema; hyperkalaemia
