Pathology Flashcards
What is a typical presentation of UTI?
Dysuria, frequency increased, smelly urine
Presentation of UTI in very young?
Unwell, failure to thrive
Presentation of UTI in very old?
Incontinence, off their feet
What is the content of normal urine?
Low pH, high osmolality and high ammonia
Is the urinary tract sterile?
Yes except for the term a urethra
Why is a initial urine sample not useful?
Because initial urine is heavily contaminated by urethral floral bacteria
What type of urine sample do we use?
MSSU (mid-stream specimen of urine0
How is MSSU cultured?
Sent to a museum hahah jk I’m losing my mind
Dip slide method (agar and moist sponge) 24hr incubation at 37degrees
At what level of a MSSU culture is there an infection?
10(5) Per ml
Is there an infection in MSSU culture is 10(3)-10(4)
If symptoms probably an infection, if no symptoms 50% chance
Problems with MSSU?
Difficult to collect in young children and elderly and
Some bacteria species are no not normally present in terminal urethra/ rectal flora and may be pathogenic at low colony numbers
What bacteria commonly causes a UTI?
E.coli
What is urethritis
Urethra inflammation
What is cystitis
Bladder inflammation
What is ureteritis
Is inflammation of ureter
What is acute pyelonephritis?
Inflammation of kidney
What are the predisposing factors to a UTI?
Stasis of urine, pushing bacteria up urethra from below, generalised predisposition to infection
What causes stasis of urine?
Obstruction or loss of “feeling” of full bladder
What are causes of pushing bacteria up urethra from below?
Sexual activity in females and catheterisation
Why is stasis of urine a predisposing factor to UTI?
Because bacteria that get higher up don’t get flushed out
What happens int he urinary system if there is a urethra obstruction?
There is upper urethral and bladder dilatation, causing bilateral hydroureter causing bilateral hydronephrosis and eventually chronic renal failure
What are consequences of obstruction within the urinary system?
Proximal dilatation, there is slowed urine flow causing bacteria not being able to be flushed out and causing an infection, sediments also form due to slowed urine flow creating calculous which cause additional obstruction
Major renal tract abnormality causing a UTI in a child?
Vesicoureteric reflux
What is vesicoureteric reflux?
Decreased angulation of ureter entering the bladder
Common cause of obstruction of renal tract in adult male?
Benign prostatic hyperplasia
Common cause of obstruction of renal tract in adult female?
Uterine prolapse
Common cause of obstruction of renal tract in both sexes?
Tumours and calculus
Why does a spinal cord/ brain injury cause stasis of urine?
There is decreased sensation, so there is no sense of when to micturate and no sense of when bladder is completely empty soo urine in bladder (residual volume) causing stasis of urine
Why is the female sex predisposed to getting UTIs from bacteria being pushed up the urethra from below?
Short urethra,
Lack of prostatic bacteriostatic secretion,
Closeness of urethral orifice to rectum,
Sexual activity,
Pregnancy (puts pressure on ureters and bladder0
Acute complication of a UTI?
Severe sepsis and septic shock
Chronic complication of UTI
Chronic pyelonephritis which can cause hypertension and chronic renal failure
Or calculi can cause obstruction, causing hydronephrosis, which will cause hypertension and chronic renal failure
What are mesangial cells?
“Tree-like” group of cells that support capillaries
What does the efferent arteriole contain ?
Plasm, unfiltered proteins such as albumin and antibodies
What is glomerulonephritis?
Disease of the glomerulus
What are the 4 common presentations of glomerulonephritis?
Haematuria, heavy proteinuria, slowly increasing proteinuria, acute renal failure
Main causes of haematuria?
UTI, urinary tract stone, urinary tract tumour, glomerulonephritis
Investigations for haematuria?
Urine culture, ultrasound, check results then check his clotting and proceed to renal biopsy
What is IgA glomerulonephritis?
IgA is stuck within the mesangium, clogging up with mesangium with IgA, the IgA irrritates the mesangial cells causing them to proliferate and produce more matrix
In IgA glomerulonephritis what would you expect to see in light microscopy?
Acccumulation of pink mesangial matrix and too many mesangial cells
In IgA glomerulonephritis what would you expect to see in immunoflourescence?
IgA immunoglobulin and complement component C3 in mesangial area of all glomeruli
In IgA glomerulonephritis what would you expect to see in electron microscopy?
Deposits of IgA with prominent mesangial cells, the IgA cause increased proliferation of mesangial cells
What is IgA nephropathy prognosis?
Return to normal as usually self-limiting, a small % go onto develop chronic renal failure via continued deposition of matrix
What is membranous glomerulonephritis
Thickened glomerular basement membrane due to IgG deposits between basal lamina and podocyte, causing protein in the urine
What does membranous glomerulonephritis look like on light microscopy?
Thickened glomerular basement membrane
What does membranous glomerulonephritis look like on silver stain microscopy?
Spikes of new basement membrane matrix material underneath podcytes
What does membranous glomerulonephritis look like on electron microscopy?
Deposits of IgG, basal lamina spike and thickened membrane
What affect does IgG have between the basal lamina and podocyte?
IgG activates complement (C3) which punches holes in the filter, creating a leaky filter that allows albumin to be filtered into urine causing nephrotic syndrome
Cause of diabetic glomerulonephritis?
There is glycated molecules causing matrix deposition in basal lamina underlying the endothelium and in mesangial matrix, this causes thickened but leaky basement membranes and the mesangial matrix compresses the capillaries
What would diabetic nephropathy look like on light microscopy
Small compressed capillary lumens, adhesions to Bowmans capsules, thickened capillary wall which is leaking albumin, increased mesangial matrix (which compresses capillaries), thickened narrowed arterioles (reduced blood flow to glomerulus)
What is nodules of mesangial matrix a sign of?
Kimmelsteil-Wilson lesion
What does rapidly rising creatinine represent/
Acute renal failure
What does crescentic glomerulonephritis look like in histology
Early endothelial damage with fibrin deposition, cellular proliferation and influx of acrophages (forming a crescent) around glomerular tuft, within the Bowman’s space
What are the causes of crescentic glomerulonephritis?
Granulomatosis with polyangiitis, microscopic polyarteritis, antiglomerular basement membrane disease, other forms of glomerulonephritis
What is granulomatosis with polyangiitis?
A form of vasculitis which affects vessels in the kidneys, nose and lung
What antibodies can you test for in granulomatosis with polyangiiits?
Presence of anti-neutrophil cytoplasmic antibodies (ANCA)
What do anti-neutrophil cytoplasmic antibodies do within the body/
They are directed against proteinase 3 and myeloperoxidase, antibodies produce tissue damage via interaction with primed neutrophils and endothelial cells
Granulomatosis with polyangiitis prognosis?
Fatal if left untreated, 75% complete remission with cyclophosphamide
What staging criteria is used for ACute Kidney Injury?
RIFLE
Definition of risk of acute kidney injury?
Increase in serum creatinine level (1.5x) or decrease in GFR by 25% or UO <0.5ml/kg/h for 6 hours
Definition of Injury of kidneys, a stage in acute kidney injury/
Increase in serum creatinine level (2x) or
decrease in GFR by 50% or
UO<0.5mL/kg/h for 12 hours
Definition of failure of kidneys, in acute kidney injury?
Increase in serum creatinine level (3x) or
Decrease in GFR by 75% or
Serum creatinine level >355umol/l with acute increase of >44umol/L or
<0.3ml/kg/h for 24 hours or
Anuria for 12 weeks
define the loss stage of acute kidney injury?
Persistent ARF or complete loss of kidney function >4 weeks
Define the end-stage kidney disease stage of acute kidney injury?
Complete loss of kidney function >3 months
Presentation of chronic renal failure
Asymptomatic, tiredness, anaemia, oedema, high blood pressure, bone pain due to renal bone disease, pruritus, n/v, dyspnoea, pericarditis, neuropathy, coma
Infection of ureter
Ureteritis
Iatrogenic/ trauma disease that can occur to ureter?
Inadvertently cut or tied during hysterectomy or colon resection
Neoplasia disease of the ureter?
TCC of ureter, TCC of bladder obstructing the VUJ, prostate cancer obstructing VUJ, pelvic malignancy, pelvic or para-aortic lymphadenopathy
Hereditary diseases of the ureter?
PUJ obstruction, VUJ reflux
Obstruction disease of the ureter?
Intra-luminal (stone, blood clot), intra-mural (scar tissue, TCC), extra-luminal (pelvic mass, lymph nodes)
Presentation of ureter diseases?
Pain, pyrexia, palpable mass, haematuria, renal failure
Infection disease of bladder?
Cystitis
Inflammation disease of the bladder?
Interstitial cystitis, Colombo diverticulitis resulting in colo-vesical fistula
Iatrogenic/ trauma diseases of the bladder
Bladder rupture, bladder injury from hysterectomy (resulting in vesisco-vaginal fistula)
Neoplasia disease of the bladder/
TCC of bladder, SCC of bladder
Idiopathic conditions of the bladder?
Overactive bladder syndrome
Degenerative diseases of the bladder?
Chronic urinary retention
Neurological diseases of the bladder
Neurogenic bladder dysfunction
Presentation of bladder disease
Pain, pyrexia, haematuria, lower urinary tract symptoms, recurrent UTIs, chronic urinary retention, urinary lark from vagina (vesico-vaginal fistula), pneumaturia (colo-vesical fistula)
What are storage LUTS
Frequency, nocturia, urgency, urge incontinence
What are voiding LUTS
Poor flow, intermittency, terminal dribbling
What are the common causes of LUTS
Bladder pathology, bladder outflow obstruction, pelvic floor dysfunction, neurological causes
What are some neurological causes of LUTS?
Supra-pontine lesions (stroke, Alzheimer’s, Parkinson’s),
infra-pontine supra-sacral lesions (spinal cord injury, disc prolapse, spina bifida),
Infra-sacral (multiple sclerosis, diabetes, causes equine compression, surgery to retroperitoneum)
Systemic disorders that can cause LUTS?
Chronic renal failure, cardiac failure, diabetes mellitus, diabetes insipidus
What controls bladder sesnsation and conscious inhibition of micturation?
The cortical centre
What is known as the micturation centre?
Pons
What are the sacral segments uncontrolled of micturation?
S2-S4
Relaxation of internal urethral sphincter is via what nerves?
S2-S4 autonomic- sympathetic
Relaxation of external urethral sphincter is via what nerves?
Somatic n.
Contraction of detrusor muscle is via what nerves?
Autonomic- parasympathetic
What are the 2 stages within the micturation cycle?
Storage/ filling phase ans voiding phase
Types of infection/ inflammation diseases of bladder outflow tract?
Prostatitis, balanitis
Iatrogenic/ trauma disease of the bladder outflow tract?
Pelvic floor damage after traumatic vaginal delivery or hysterectomy, urethral injury from catheterisation or pelvic fracture
Neoplasia of bladder outflow tracts?
Prostate cancer, penile cancer
Idiopathic diseases of the bladder outflow tracts?
Chronic pelvic pain syndrome
Obstruction disease of bladder outflow tract?
Primary bladder neck obstruction, benign prostatic enlargement causing obstruction, urethral stricture, mental stenosis, phimosis
Presentation of bladder outflow tract diseases?
Pain, pyrexia, haematuria, voiding LUTS (hesitancy, intermittency, poor flow, terminal dribbling, incomplete bladder emptying), overflow incontince, stress urinary incontinence, recurrent UTIs, acute urinary retention, chronic urinary retention
Why is voiding LUTS causes in bladder outflow tract disease?
Because of bladder outflow obstruction
Why is overflow incontinence a symptom of bladder oputflow tract diseases
Due to high pressure chronic urinary retention
Define acute urinary retention
Painful inability to void with a palpable and percussible bladder
What are the residuals of acute urinary retention
Vary from 500ml to 1 litre
What are some risk factors of acute urinary retention?
Benign Prostatic Obstruction, UTI, urethral stricture, alcohol excess, post-operative causes, acute surgical or medical problems
Patients with acute urinary retention due to BPO are usually triggered because of what/
Constipation, alcohol excess, post operative causes, urological procedure
What is treatment of acute urinary retention
Catheterisation
Define chronic urinary retention
Painless, palpable and percussible bladder after voiding
What are the chronic urinary retention residuals?
400ml to >2 litres
What is the main aetiological factor of chronic urinary retention?
Detrusor underactivity
How does chronic urinary retention present?
Can be asymptomatic,
LUTS,
Or as complications (UTI, bladder stones, overflow incontinence, post-renal or obstructive renal failure)
In chronic urinary retention when the bladder reaches full capacity and bladder pressure is in excess of 25cm water what symptoms can be expected/
Overflow incontinence, renal allure
What is the immediate treatment of chronic urinary retention?
Catheterisation
What are some subsequent treatment methods of chronic urinary retention?
CISC- clean intermittent self catheterisation
TURP- transurethral resection of prostate (if due to benign prostatic obstruction)
What is required to diagnosis UTI?
Microbiological evidence and symptoms/ signs
What microbiological evidence is neeeded to diagnose a UTI?
Bacterial count of 10(4)cfu/ml from MSSU specimen with no more than 2 species of micro-organisms
What symptoms/ signs are required to diagnose UTI?
At least one of the following:
Fever >38, loin/flank pain or tenderness, suprapubic pain or tenderness, urinary frequency, urinary urgency, dysuria
What are the 2 types of UTI?
Uncomplicated (young sexually active females) or Complicated (everyone else)
What types of organisms can cause UTIs?
E.coli, staph. Saprophyticus, klebsiella, proteus, pseudomonas, staph aureus
What complications can occur from UTIs?
Infection: sepsis (especially in pyelonephritis), perinephric abscess, renal failure, bladder malignancy (SCC), acute urinary retention, frank haematuria, bladder of renal stones
What investigations are used to diagnose a UTI?
MSSU/ CSU
Lower tract- flow studies, residual bladder scan, cystoscopy
Upper tract- USS kidneys, IVU/CT- KUB, MAG-3 renogram, DMSA scan
Name some emergencies related to urinary tract diseases?
Acute renal failure, sepsis due to UTI, renal colic, severe haematuria, metastatic disease causing metabolic derangements, acute urinary retention, chronic high-pressure urinary retention, iatrogenic injury/ trauma, testicular torsion, paraphimosis, priapism
What are the methods for measuring excretory renal function
Inulin clearance, isotope GFR, 24hr urine collection plus blood test, GFR estimating equations
What is creatinine generated from?
Breakdown of muscle
What factors need to be taken into account when measuring the GFR with serum creatinine?
Age, ethnicity, gender, weight, other isssues eg liver disease
What is the formula for COckgroft Gault
{[140-age]x weight x 1.23)/ SCr x (0.85 if female)
What is the formula for MDRD 4 variable equation?
If someone has a GFR of >90ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 1:
Kidney damage/ normal or high GFR
If someone has a GFR of 60-89ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 2
Kidney damage/ mild retention in GFR
If someone has a GFR of 45-59ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 3a
Moderately impaired
If someone has a GFR of 30-44ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 3b
Moderately impaired
If someone has a GFR of 15-29ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 4
Severely impaired
If someone has a GFR of <15ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 5
Advanced or on dialysis
What can freely cross the GBM?
Water, electrolytes, urea, creatinine
What crosses the GBM but is reabsorbed in the proximal tubule?
Glucose, low molecular weight proteins (alpha2 microglobulin)
What does not cross the GBM?
Cells (RBC, WBC), high molecular weight proteins (albumin, globulins)
How can you assess kidney filtering function
Urinalysis (dipstick), protein quantification (PCR, ACR)
Define Chronic kidney disease?
Presence of kidney damage (abnormal blood, urine or x-ray findings) or
GFR<60ml/min/1.73m2
That is present for >/= to 3 months
Name some common aetiology of CKD?
Diabetes, glomerulonephritis, hypertension, renovascular disease, polycystic kidney disease
What is the clinical approach taken to chronic kidney disease?
Detection of the underlying aetiology:
-treat the specific disease
Slowing the rate of renal declin:
-genetic therapies
Assessment of complications related to reduced GFR:
-prevention and treatment
Preparation for renal replacement therapy
Symptoms of chronic kidney disease?
Anaemia-pallor, hypertension, SOB, itch and cramps, cognitive changes- language and attention, anorexia, vomiting, taste disturbance, uraemia odour, polyuria or oliguria, nocturia, haematuria, proteinuria, peripeheral oedema
With someone with chronic kidney disease, what could the kidney look like on ultrasound?
Bilaterally small with thinned cortices suggesting intrinsic disease (eg glomerulonephritis),
Unilateral small Kidney which may indicate renal arterial disease,
Clubbed calyces and cortical scars suggesting reflux with chronic infection or ischameia,
Enlarged cystic kidneys suggesting cystic kidney disease
How would you manage slowing the rate of renal decline, in someone with chronic kidney disease?
BP control, Control proteinuria (ACE inhibitors/ ARBs), treat underlying cause
What are some complications that are related to reduced GFR?
Acidosis, anaemia, bone disease, CV risk, death and dialysis, electrolytes, fluid overload, gout, hypertension, iatrogenic issues
How to manage the complications related to reduced GFR?
Acidosis- bicarbonate
Anaemia- Erythropoietin and iron
Bone disease- diet and phosphate binders
CV risk- BP, aspirin, cholesterol, exercise, weight
Death and dialysis- counsel and prepare
Electrolytes- diet and consider drugs
Fluid overload- salt and fluid restriction, diuretics
Gout- optimise +/- meds
Hypertension- weight, diet, fluid balance, drugs
Preparation needed for end stage renal disease and renal replacement therapy
Education and information, selection of modality (HD, PD, transplant), planning access, deciding when to start RRT and MDT
what is glomerulonephritis?
An inflammatory disorder of the kidney which is classified based on morphology
Glomerulonephritis common features?
Haematuria, proteinuria, hypertension, renal insufficiency
What can be the source of haematuria?
Kidney, ureter, bladder, prostate, urethra
In which condition could you expect to see haematuria more? Nephrotic or nephritic?
Nephrotic
Is renal insufficiency and hypertension more common in nephritic syndrome or nephrotic?
Nephritic
Describe the presentation of nephritic state?
Active urine sediment- haematuria, dysmorphic RBCs, cellular casts,
Hypertension,
Renal impairment
Describe the presentation of nephrotic syndrome?
Oedema, proteinuria >3.5g/day, hypoalbuminemia, hyperlipidemia, can be caused by primary or secondary glomerular diseases
Name some differential diagnosis of nephrotic suyndrome?
Congestive heart failure- however will have normal albumin
Hepatic disease- however no proteinuria
What are the 2 categories that glomerulonephritis can be split into?
Proliferative or non-proliferative
What does diffuse, focal, global and segmental nomenclatures mean in relation to the glomerulus?
Diffuse >50% of glomeruli affected
Focal <50% of glomeruli affected
Global- all glomerulus affected
Segmental- part of the glomerulus affected
What are the different classes of proliferative glomerulonephritides?
Diffuse proliferative (eg post-infective nephritis), focal proliferative (eg mesangial IgA disease), focal necrotising (crescentic nephritis), membrano-proliferative nephritis
What can you expect from post infective glomerulonephritis in microscopy?
Congested cells, immune deposits and lumps
When is it common to get a post-streptococcal glomerulonephritis?
10-21 days after infection typically of throat or skin
What is the most common group that causes post-streptococcal glomerulonephritis
Lance field group A streptococci
What genes can cause a genetic predisposition to post-streptococcal glomerulonephritis?
HLA-DR, -Dp
How would you treat post-infective glomerulonephritis?
Antibiotics (debatable), loop diuretics (eg frusemide) for oedema, vasodilator drugs (eg amlodipine) for hypertension
What kind of proliferative glomerulonephritis is post-infection nephritis?
Diffuse proliferative glomerulonephritis
What kind of proliferative glomerulonephritis is IgA nephropathy
Focal proliferative
How is IgA nephropathy characterised?
IgA deposition in the mesangium + mesangial proliferation
How does IgA nephropathy present?
Microscopic haematuria + proteinuria, nephrotic syndrome and IgA crescentic glomerulonephritis
What is the prognosis for IgA nephropathy?
Up to 40% can progress to end stage kidney disease
Causes of crescentic glomerulonephritis/
Anti-neutrophil cytoplasmic antibody (ANCA)(microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis) or
Anti-glomerular basement membrane (GBM) eg anti_GBM nephritis or Goodpasture’s syndrome or
Others- IgA vasculitis, post-infective glomerulonephritis, SLE
How to treat Crescentic glomerulonephritis?
High dose steroids, cyclophosphamide, plasma exchange
How does anti-GBM disease present?
Nephritis (anti-GBMM glomerulonephritis) and nephritis + lung haemorrhage (Goodpasture’s sydnrome)
How is anti-GBM disease diagnosed?
Anti-GBM antibodies in serum and kidney
How is Anti-GBM disease treated?
Aggressive immunosuppressive: steroid, plasma exchange, cyclophosphamide
How is crescentic glomerulonephritis treated?
Immunosuppresion- corticosteroids, plasma exchange, cytotoxic eg cyclophosphamide, B-cell therapy eg rituximab, complement inhibitors
Name the types of non-proliferative glomerulonephritis?
Minimal change disease, focal and segmental glomerulonephritis, membranous nephropathy
How to you generally treat nephr0tic syndrome with regards to the common symptoms/
Loop diuretics + salt and fluid restriction (for oedema), Renin-angiotensin-aldosterone-blockade (for hypertension), Heparin or warfarin (reduced risk of thrombosis), pneumococcal vaccine (for reduced risk of infection), statins (to treat dyslipidemia)
How is minimal change nephrotic syndrome characterised?
Common in children, sudden onset of oedema in days, proteinuria
Is there a high relapse rate in minimal change nephrotic syndrome?
Yes, 2/3rd of patients relapse
How is minimal change disease treated/
Prednisolone (1mg/kg for up to 16 weeks), once remission is achieved there is a slow taper over 6 months.
The initial relapse is treated with further steroid course, however if relapse again, it is treated with:
Cyclophosphamide, cyclosporine, tacrolimus, mycophenolate mofetil, rituximab
What is minimal change disease’s prognosis?
Relapse common but risk of end stage kidney disease is low,
Steroid toxicity can occur due to multiple exposure to steroids
What is normal serum albumin levels?
> 35g/l
How does focal and segmental glomerulonephritis present?
Nephrotic syndrome
What does pathology reveal for focal and segmental glomerulonephritis
Reveals focal and segmental sclerosis with distinctive patterns:
Tip lesion, collapsing, cellular perihilar
What is the prognosis of focal and segmental glomerulonephritis?
High chance of progression to end stage kidney disease
What is the treatment of focal and segmental glomerulosclerosis?
General mesasure, trail of steroids (gerneally steroid resistant), cyclosporin, cyclophosphamide, and rituximab
What is membranous nephropathy
Commonest cause of nephrotic syndrome in adults, can be idiopathic or associated with other infections/ diseases. Renal biopsy shoes diffuse global subepithelial deposits within the glomerulus
What are the serological markers of membranous nephropathy?
Anti-phospholipase A2 receptor (PLA2R) antibody positive,
THrombospondin type 1 domain containing 7A (THSD7A)
What are some possible secondary causes of membranous nephropathy?
Malignancies, SLE, rheumatoid arthritis, drugs (NSAIDs, gold, penicillamine)
How to treat membranous nephropathy?
General measure for at least 6 months, use immune suppression if symptomatic nephrotic syndrome or rising proteinuria or deteriorating renal function,
Cyclophosphamide and steroids (alternate months) for 6 months, cyclosporin,
Rituximab
What is the prognosis of membranous nephropathy?
Resolved spontaneously in a third of patients,
Good in treated patients whose proteinuria resolves
About 25% are on dialysis at 10 years and
Can recur in renal transplants
Define acute renal failure?
Rapid loss of glomerular filtration and tubular function over hours to days, resulting in the retention of urea/ creatine and sometimes oliguria
Define AKI stage 1 using KDIGO criteria?
Increase in serum creatinine:
1.5-1.9 times baseline in the past 7 days OR
>/=26.5umol/l increase
AND
<0.5ml/kg/h urine output for 6-12hours
Define AKI stage 2 using KDIGO criteria?
Increase in serum creatinine:
2.0-2.9 times baseline in the past 7 days
AND
<0.5ml/kg/h urine output for >/=12hours
Define AKI stage 3 using KDIGO criteria?
Increase in serum creatinine:
3.0 times baseline in the past 7 days OR
>/=354umol/l increase OR
Initiation of renal replacement therapy
AND
<0.3ml/kg/h urine output for >/=24hours OR
Anuria for >/12 hours
What are the dangerous consequences of AKI?
Acidosis Electrolyte imbalance Intoxication Overload Uraemic complications
(AEIOU)
What are the 3 groups of causes of AKI?
Pre-renal (blood flow to kidney)
Renal (damage to parenchyma)
Post-renal (obstruction to urine exit)
Name some intrinsic causes of AKI?
Acute tubular injury: Prolonged pre-renal AKI, rhabdomyolysis, haemoglobinuria, nephrotoxins Tubulointerstitial injury, Glomerulonephritis, Myeloma, Vasculitis: Lupus, ANCA associated, Acute tubular necrosis
Pre-renal causes of AKI?
Sepsis, hypovolaemia (haemorrhage, burns, vomiting/ diarrhoea, diuretics, dehydration), hepatorenal syndrome, cardiac failure, hypotension (medications), shock, liver failure, arterial occlusion, vasomotor (NSAIDs/ACE inhibitors)
Post-renal causes of AKI?
Obstruction:
Intraluminal- calculus, clot, sloughed papilla
Intramural- malignancy, ureteric stricture, radiation fibrosis, prostate disease
Extramural- RPF, malignancy
What are the risk factors for Radiocontrast nephropathy
DM, renovascular disease, impaired renal function, paraprotein, high volume of radiocontrast
What presentation can you expect from renal dailure in myeloma?
Cast nephropathy, light chain nephropathy, amyloidosis, hypercalcaemia, hyperuricaemia
Blood tests to be completed for AKI?
U&Es, bicarbonate, LFTs, bone, FBC, clotting
What are the risk factors for AKI?
Age >75, Previous AKI,l Heart failure, Liver failure, Chronic kidney disease, DM, Vascular disease, Cognitive impairement
What are some risk events of AKI?
Sepsis (eg pneumonia, cellulitis, UTI),
Toxins (eg X-ray contrast, NSAIDs, gentamicin, herbal remedies)
Hypotension (eg relative to baseline blood pressure),
Hypovolaemia,
Major surgery
What is the STOP AKI prevention care bundle?
S- sepsis
T- toxins: avoid (eg Gentamicin, NSAIDs, IV iodinated contrast)
O- optimise BP and volume status
P- prevent harm (daily U&Es, fluid balance and medication review
If sepsis is suspected, what steps are suggested?
Sepsis 6, Blood cultures, urine output monitoring and U&Es, Fluids, Antibiotics, Lactate level, Oxygen saturation monitoring
If a patient is hypovolaemic, what fluids would you suggest?
IV fluids- resuscitation fluids 250-500mls IV crystalloid bolus over 15 mins and review response
If the AKI is a post-renal problem what is a good starting management?
A catheter
What are the 5Rs for IV prescribing?
Rescuscitation- urgent to restore circulation
Routine maintenance- If cannot take orally
Replacement- additional to maintain
Redistribution- abnormal internal fluid resdistribution
REASSESSMENT
What is normal fluid intake and output?
2500ml intake
2100-2600 output
What is an early sign of hyperkalaemia on an ECG?
Peaked T waves
What are signs of hyperkalaemia on an ECG?
Peaked T waves, P wave widens and flattens, PR segment lengthens, P waves eventually disappear, Prolonged QRS internal, High grade AV block, Conduction block, Sinus bradycardia
Hyperkalaemia treatment?
Calcium gluconate (stabilise myocardium) Salbutamol and insulin-dextrose (to shift K+ intracellularly) Diuretics, dialysis, anion exchange resins (to remove)
How to treat intoxication from AKI?
Morphine, digoxin
Advantages of HD?
Rapid solute removal,
Rapid volume removal,
Rapid correction of electrolyte disturbances,
Efficient treatment for hypercatabolic patient
Disadvantages of HD?
Haemodynamic instability,
Concern if dialysis associated with hypotension,
Fluid removal only during short treatment time
Advantages of CRRT?
Slow volume removal associated with greater haemodynamic stability,
Absence of fluctuation in volume and solute control over time,
Greater control over volume status
Disadvantages of CRRT
Need for continuous anticoagulation, may delay weaning/ mobilisation, may not have adequate clearance in hypercatabolic patient
Define End-stage renal disease
Irreversible damage to a persons kidneys so severely affecting their ability to remove or adjust blood wastes that, to maintain life, they must have either dialysis or a kidney transplant
What is the syndrome of advanced CKD called?
Uraemia
How big is anormal prostate?
15cc, increases with age
Wha are the McNeal’s Prostatic zones?
Transition, central, peripheral and anterior fibromusclar stroma zones
What is Benign prostatic hyperplasia?
Fibromuscular and glandular hyperplasia of the prostate, predominantly affecting the transition zone, it is part of aging process in men
Symptoms of benign prostatic hyperplasia?
Moderate to severe LUTS in 50% of men
What do they look at in the international prostate symptom score sheet?
Incomplete emptying, frequency, intermittency, urgency, weak stream, straining, nocturia
What is classed as mild, moderate and severe in the international prostate symptom score sheet?
Mild: 0-7,
Moderate: 8-19
severe: >/=20
How can you assess LUTS?
Symptom scoring systems, frequency volume charts
Symptoms of voiding LUTS
Hesitancy, poor stream, terminal dribbling, incomplete emptying
Symptoms of storage LUTS?
Frequency, nocturia, urgency +/- urge incontinece
If you believe someone has a prostate problem what examinations would you complete?
Abdomen: ? Palpable bladder Penis: ? External urethral mental stricture, ? Phimosis DRE: Assess prostate size and consistency, ? Suspicious nodules or firmness Urinalysis: ? Blood, ? Signs of UTI
Investigations if you beleive someone has a prostate problem?
MSSU, FLow rate study, Post-void bladder residual USS, Bloods- PSA, urea and creatinine, Reanal tract USS, Flexible cytoscopy, Urodynamic studies, TRUS-guided prostate biopsy
At was level of Qmax do you have a big chance of BOO?
Qmax <10ml/s
90% chance of BOO
Treatment of uncomplicated BPO?
Waiting, Alpha blockers, 5 alpha reductase inhibitors, TURP, Open retro public or transvesical prostatectomy, Endoscopic ablative procedures
How do alpha blockers work in BPO?
The sympathetic alpha-adrenergic nerves innervate the smooth muscle of bladder neck and prostate, so the alpha blockers cause smooth muscle realisation and antagonise the “dynamic” element to prostatic obstruction
What are the types of alpha blockers?
Non-selective: phenoxybenzamine
Selective short acting: prazosin, indoramin
Selective long acting: alfuzosin, doxazosin, terazosin
Highly selective: tamsulosin
How do 5a-reductase inhibitors work?
5a-reductase converts testosterone to dihydrotestosterone
So 5a reductase inhibitors block this and reduce prostate size and reduce risks of progression of BPE, reduce LUTS and reduce prostatic bleeding
Side effects of 5a-reductase inhibitors?
Impaired sexual function, breast growth
Name the 2 5a-reductase inhibitors currently available?
Finasteride (5AR type II inhibitor)
Dutasteride (5AR type I and II inhibitor)
What is TURP?
Transurethral resection of prostate
complications of TURP?
Bleeding, infection, retrograde ejactulation, stress urinary incontinence, prostatic regrowth causing recurrrent haematuria or BOO
Alternative surgical procedures used for BPO?
Transurethral laser vaporisation, urolift
Complications of BOO?
Progression of LUTS, acute urinary retention, chronic urinary retention, urinary incontinence (overflow), UTI, bladder stone, renal failure from obstructed ureteric outflow due to high bladder pressure
Treatment of Complicated BOO?
Cystolitholapaxy and TURP (BPO and bladder stones),
Long term urethral or suprapubic catheterisation, clean intermittent self-catheterisation
Treatment of acute urinary retention?
Catherterisation, if no renal failure alpha blocker and remove catheter in e days
Complications from acute urinary retention?
UTI, post-decompression haematuria, pathological duresis, renal failure and electrolyte abnormalities
What is the main aetiological factor causing chronic urinary retention?
Detrusor underactivity
Complications of chronic urinary retention/
UTI, post0decompression haematuria, pathological diuresis, electrolyte abnormalities, persistent renal dysfunction
What are the features of pathological diuresis?
Urine output >200ml/hr + postural hypotension+ weight loss + electrolyte disturbance
Intrinsic causes of obstructuion at PUJ?
Stone, ureteric tumour, blood clot,fungal ball
Extrinsic causes of obstruction at PUJ?
Crossing vessels au PUJ, lymph nodes (tumour), abdominal mass (tumour)
Intrinsic causes of a obstruction at the ureter
Stone, ureteric tumour, scar tissue, blood clot, fungal ball
Extrinsic causes of a obstruction at the ureter
Lymph nodes (tumour, retroperitoneal fibrosis), iatrogenic, abdominal/ pelvic mass (tumour, pregnant uterus)
Intrinsic causes of a obstruction at the VUJ?
Stone, bladder tumour, ureteric tumour
Extrinsic causes of a obstruction at the VUJ
Cervical tumour, prostate cancer
Symptoms of upper urinary tract obstruction?
Pain, frank haematuria, symptoms of complications
Signs of upper urinary tract obstruction?
Palpable mass, microscopic haematuria, signs of complications
Complications of upper urinary tract obstruction?
Infection and sepsis, renal failure
Treatment of Upper urinary tract obstruction?
Emergency treatment of obstruction; percutaneous nephrostomy insertion or retrograde stent insertion
treat underlying cause:
Stone- ureteroscopy and laser lithotripsy +/- basketing or ESWL
Ureteric tumour- radial nephro-ureterectomy
PUJ obstruction- laparoscopic pyeloplasty
What is a nephrostomy?
Percutaneous puncture + tube
Describe a ureteric stent?
Silicone, polyurethane, nickel titanium stent inserted into ureter, causing dilation
Lower urianry tract obstruction presentation?
LUTS, acute urinary retention, chronic retention, recurrent UTI and sepsis, frank haematuria, formation of bladder stones, renal failure
Emergency treatment of lower urinary tract obstruction
Urethral/ suprapubic catheterisation
Definitive treatment of lower urinary tract obstruction?
Treat underlying cause: BPE-TURP, Urethral stricture- optical urethrotomy, Meatal stenosis- meatal dilatation, Phimosis- circumcision
High pressure chronic urinary retention presentation?
Painless, incontinent, raised creatinine, bilateral hydro-nephrosis
Low pressure chronic urinary retention?
Painless, dry, normal creatinine, normal kidneys
Complications of urinary retention?
Decompression haematuria, post obstructive diuresis
Describe decompression of haematuria?
Shearing of small vessels due to differing compliance of tissue layers, self limiting
Describe post obstructive diuresis?
Greater than 200ml/hr, can lead to life threatening Na and H2O depletion
Most common site of urothelial tumours?
Bladder- 90%
Risk factors for transitional cell carcinoma of the bladder
Smoking, aromatic amines, non-hereditary genetic abnormalities
Risk factors for squamous cell carcinoma
Schistosomiasis (S.haematobium only), chronic cystitis, cyclopjosphamide therapy, pelvic radiotherapy,
Adenocarcinoma- urachal
Bladder cancer presentation?
Painless visible haematuria,
Symptoms due to invasive or metastatic disease
Haematuria may be frank or microscopic,
Recurrent UTI,
Storage bladder symptoms- dysuria, frequency, nocturia +/- urge incontinence, bladder pain- suspect CIS
Investigations of haematuria?
Urine culture, CT urogram (IVU), ultrasound scans, cystourethroscopy, urine cytology, BP and U&E’s
If someone has frank haematuria within wheat time should they have a flexible cystourethroscopy?
Within 2 weeks
If someone has microscopic haematuria within what time should they have a flexible cystourethroscopy?
Within 4-6 weeks
Describe the grades of TCC
G1- well diff- commonly non-invasive,
G2- mod diff- often non-invasive,
G3- poorly diff- often invasive,
Carcinoma in situ
A what T stages of bladder TCC is it muscular invasive?
T2a and above
Low grade non-muscular invasive bladder cancer treatment?
Endoscopic resection + single insillation of intravesical chemotherapy within 24hours,
Need endoscopic follow up,
Can consider prolonged course of intravesical chemotherapy
High grade non-muscle invasion bladder cancer or CIS treatment
Endoscopic resection not sufficient,
Consider intravesical BCG therapy,
If refractory to BCG- need radical surgery
Muscle invasive bladder cancer treatment?
Neoadjuvant chemotherapy, followed by…
Radical radiotherapy and/or,
Radical cystoprostatectomy (men) or anterior pelvic exenteration with urethrectomy (women), with extended lympahdenectomy and/ or
Radical surgery combined with i continent urinary diversion (ileal) conduit, continent diversion (bowel pouch with catheterisable stoma) or orthotopic bladder substitution
Upper tract TCC presenting features?
Frank haematuria, unilateral ureteric obstruction, Flank or loin pain, Symptoms of nodal or metastatic disease: Bone pain, hypercalcaemia, lung, brain
Upper tract TCC diagnostic investigations?
CT-IVU (CT urogram), urine cytology, ureteroscopy and biopsy
How does a CT-IVU Diagnosis a upper tract urothelial cancer?
It shows a filling defect in the renal pelvis
Treatment for Upper Tract Urothelial cancer
Nephro-ureterectomy
Indications fo nephron-sparing endoscopic treatment in upper tract urothelial cancer?
If unfit for nephro-ureterectomy or has bilateral disease,
So get ureteroscopy can lasers ablation
Will needed regular surveillance ureteroscopy
Why do all cases of upper tract urothelial cancer need surveillance cystoscopy?
Because there is a high risk of synchronous and metachronous bladder TCC
Types of benign renal tumours?
Oncocytoma, angiomylipoma
Histological subtypes of renal adenocarcinoma?
Clear cells, papillary, chromophobe, Bellini type dictaphone carcinoma
Risk factors of renal adenocarcinoma?
Family history (vHL, familial clear cell RCC, hereditary papillae RCC), smoking, anti-hypertensive medication, obesity, end-stage renal failure, acquired renal cystic disease
Presentation of renal adenocarcinoma?
Asymptomatic- 50% present
Flank pain, mass and haematuria- 10% present
Paraneoplastic syndrome: anorexia, cachexia, pyrexia, hypertension, hypercalcaemia and abnormal LFTs, anaemia, polycythaemia and raised ESR - 30%
MEtastatic disease: bone, brain, lungs, liver -30%
TNM staging of renal cancer
T1- tumour <7cm confined within the renal capsule
T2- tumour >7cm and confined within capsule
T3- Local extension outside capsule
T3a-into adrenal or peri-renal fat
T3b- intro renal vein or IVC below diaphragm
T3c- Tumour thrombus in IVC extends above diaphragm
T4- tumour invades beyond Gerota’s fascia
Renal adenocarcinoma spread methods?
Direct spread (invasion) through the renal capsule, venous invasion to renal vein and vena cava, haematogenous spread to lungs and bones and lymphacic spread to paracaval nodes
Renal adenocarcinoma investigations?
CT scan of abdomen and chest, provides radiological diagnosis and complete TNM staging, assess contra lateral kidney
Bloods: U+Es, FBC, LFTs,
Ultrasound, DMSA or MAG-3 renogram
Treatment of renal adenocarcinoma?
Laparoscopic radial nephrectomy,
Palliative cytreductive nephrectomy
Renal adenocarcinoma with metastases treatment?
RCC is radioresistant and chemoresistant so treat with multitargeted receptor tyrosine kinase inhibitors (suntinib, sorafenib, panzopanib, temsirolimus),
Immunotherapy (interferon alpha, interleukin-1)
What muscle do the ureters pass by?
Psoas major
What is the trig one in the bladder?
A triangular area between the ureteric and urethral orifices
Indications for renal imaging?
Renal colic and renal stone disease, haematuria, suspected renal mass, UTIs, hypertension
Contrast imaging studies used to view KUB?
IV urogram, Pyelography, micturating cystourethrography
What is a pyelography?
Injection of contrast into the ureters
What would you use a Doppler ultrasound for?
Renal artery stenosis
Isotope scans used for renal diseases, and why they are used?
DMSA- to look for renal scarring
MAG3- assess renal function and drainage
Bone scan- metastatic disease
What is the best imaging modality to diagnose renal tract stones and stage renal tumours?
CT
Types of urinary stones?
Calcium oxalate, calcium oxalate + phosphate, “triple phosphate”, calcium phosphate, Utica acid, cystine
What is the most common type of urinary stone?
Calcium oxalate
Symptoms and signs of urinary stones?
Renal pain, ureteric colic (radiating to groin), Dysuria/ haematuria/ testicular or vulval pain, Urinary infection, Loin tenderness, Pyrexia
Investigations for urinary stones?
Blood tests- FBC, U&E, creatinine, Calcium, albumin, urate, Parathormone, Urine analysis and culture, 24hr urine collections, Radiology- ultrasound KUB, IVU, CT KUB,
Indications for surgical treatment for urinary stones?
Obstruction, Recurrent gross haematuria, Recurrent pain and infection, Progressive loss of kidney function, Patient occupation
Types of surgical treatment for urinary stones?
Open surgery, endoscopic surgery, Extracorporeal Shock Wave Lithotripsy (ESWL), Percutaneous nephrolithotomy (PCNL)
Indications for open surgery for urinary stones?
Non functioning infected kidney with large stones,
For technical reasons cannot be managed another way
Types of o[pen surgery for urinary stone removal?
Simple pyelolithotomy, simple radial partial or total nephrotomy
When would toy complete a simple partial or total nephrectomy for urinary stones?
If
A non functioning kidney with large staghorn stones or
Elderly frail patients with complex stones and normal contralateral kidney
Indications for a percutaneous nephrolithotomy?
Large stone burden, associated PUJ stenosis, infundibular stricture, calyceal diverticulum, morbid obesity or skeletal deformity, ESWL resistant stones eg cystine
Contraindications for PCNL
Uncorrected coagulopathy, active UTI, obesity or unusual body habitus unsuitable for X-ray tables, relative contraindications include small kidneys and severe perirenal fibrosis
Local complications of PCNL?
Pseudoaneurysm or AV fistula,
UT injury: pelvic tear, ureteral tear, stricture of PUJ
Injury’s that can occur to adjacent organs due to PCNL?
Bowel injury,
Pneumothorax,
Systemic complications of PCNL?
Fever, sepsis, MI
What is ESWL?
Extracorporeal Shock Wave Lithotripsy
When is ESWL not effective?
Stones >2cms,
Less effective for lower pole stones,
Not effective after 2 treatments,
Ineffective for treating cystine stones
Indications for ureteroscopy?
Sever obstruction, uncontrolled pain, Persistent haematuria, Lack of progression, Failed ESWL, Patient occupation
Minor complications of ureteroscopy?
Haematuria, fever, small ureteric perforation, minor vesico-ureteric reflux
Major complications of ureteroscopy?
Major ureteric perforation,
Ureteric avulsion,
Ureteral necrosis and stricture formation
Bladder stones presentation?
Suprapubic/groin/ penile pain, Dysuria, frequency, haematuria, Urinary infection persistent, Sudden interruption of urinary stream, Usually secondary to outflow obstruction
Name the types of aorta/large vessel arteritis
Takayasu arteritis, giant cell arteritis
Name the types of medium artery vasculitis?
Polyarteritis nodosa,
Kawasaki disease
Name the types of small vessel vasculitis?
Granulomatosis polyarteritis,
Microscopic polyarteritis,
Churg-Strauss syndrome
Describe granulomatosis polyangiitis?
A granulomatous inflammtion in the respiratory tract, type of focal necrotising inflammation with crescents, more common in males and the age group 40-60y
Describe the systems affect3ed by granulomatosis polyangiitis and the subsequent symptoms?
Upper Resiratpry tract- epistaxis, basal deformity, sinusitis, deafness
Lower respiratory tract- cough, dyspnoea, haemoptysis, pulmonary haemorrhage
Kidney- glomerulonephritis
Joints- arthralgia, myalgia,
Eyes- scleritis
Heart- pericarditis
Systemic- fever, weight loss, vasculitic skin rash
Diagnostic tests for vasculitis
Urine (blood/proteins),
Renal function (raised urea/creatinine)
Biochemistry (raised alkaline phosphate, CRP, low albumin)
Haematology (anaemia, thrombocytosis, leukocytosis)
Immunology (hyperglobulinaemia, positive ANCA)
renal biopsy
The ANCA that’s diagnosis for granulomatosis polyangiitis?
C-ANCA
The ANCA that’s diagnosis for microscopic polyarteritis
P-ANCA
Infections that cause infective endocarditis?
Staphylococcus aureus, Vivian’s streptococci, enterococci
How does infective endocarditis lead to affecting the kidney
It leads to glomerulonephritis +/- vessel vasculitis due to immune complex function
If a patient has infective endocarditis, how can you tell that the renal system is affected?
Abnormal urea/creatinine
Haematuria, red cell casts,
Reduced complement levels
What is multiple myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
What are the clinical features of multiple myeloma?
Markedly elevated ESR, Anaemia, Weight loss, Fractures, Infections, Back pain/ cord compression
How is multiple myeloma diagnosed?
Bone marrow aspirate >10% clonal plasam cells,
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones protein,
Skeletal survey- lytic lesion
Presentation of renal failure in myeloma
Cast nephropathy- “myeloma kidney” Light chain nephropathy, Amyloidosis, Hypercalcaemia, Hyperuriacaemia
What history points could make you suspect systemic disease with renal involvement?
Fever, malaise, weight loss, arthralgia, myalgia, skin rash, gritty eyes, breathlessness, haemoptysis, epistaxis, haematuria, oedema
What signs would you expect if you suspected systemic disease with renal involvement?
Hands- splinter haemorrhages, purpura, Raynaud’s
Face- scleritis, uveitis, nasal cartilage deformity, retinal vasculitis, hypertensive retinopathy
Skin- vasculitic rash, scleroderma
CVS- hypertension, murmur
Chest- crepitations, haemoptysis,
Locomotor- joint swelling, tenderness
CNS- stroke, enccephalopathy
Peak age group for prostate cancer?
50-70
What is the diagnostic triad of prostate cancer?
PSA, DRE, TRUS-guided prostate biopsies
What is the normal serum range of PSA?
0-4.0ug/ml <50 yrs- 2.5 is upper limit, 50-60 - 3.5, 60-70- 4.5 >70- 6.5
What can cause elevation in PSA?
UTI, Chronic prostatitis, Instrumentatio eg cateterisation) Physiological (eg ejaculation) Recent urological procedure BPH Prostate cancer
What is the half life of PSA?
2.2 days
What is the Gleason Grading of prostate cancer?
Score biggest and second biggest area of tumour a score of 3-5 (well to poorly differentiated) and add together the scores
What are the 4 stages of prostate cancer?
Localised stage, locally advanced stage, metastasic stage, hormone refractory stage
How would you stage a localised prostate cancer?
DRE, PSA, transrectal US guided biopsies, CT, MRI
Treatment of localised prostate cancer?
Watchful waiting, Radiotherapy (external-beam, brachytherapy) Radical prostatectomy (open, laparoscopic, robotic)
Treatment of locally advanced prostate cancer?
Watchful waiting,
Hormone therapy followed by surgery,
Hormone therapy followed by radiation,
Hormone therapy alone
Types of hormonal therapy for prostate cancer?
Surgical castration: Bilateral orchidectomy Medical castration: LHRH analogues- goserelin, leuprorelin LHRH antagonists Anti-androgens Oestrogens- diethylstilboestrol
How does oestrogens help on prostate cancer?
Inhibitots LHRH and testosterone secretion,
Inactivates androgens
Direct cytotoxic effect on prostatic epithelial cells
What is the PSA level at localised, locally advanced and metastatic prostate cancer?
localised <20
Locally advanced 20-100
Metastatic- >100
How does testicular cancer nornmally present?
Painless lump
What are some other presentations of testicular cancer other than painless lump?
Tender inflamed swelling, history of trauma
Risk factors of testicular cancer?
3rd decade, Caucasians
Testicular maldescent, infertility, strophic testis, previous cancer in contrallateral testis,
Testicular germ cell neoplasia in situ is a precursor lesion
What are the types of testicular cancer tumour markers?
AFP (alpha-fetoprotein) (teratoma)
BHCG (Human Chorionic Gonadotrophin)(seminoma)
LDH (lactate dehydrogenase)
Testicular cancer investigations?
MSSU, testicular ultrasound scan and CXR, tumour markers
Treatment of testicular cancer?
Radical orchidectomy
Lymphatic drainage of testis?
Para-aortic lymph nodes
Types of testicular germ cell tumours?
Seminomatous GCT (classical, spermatocytic or anaplasic)- normally affects 30- 40yrs Non seminomatous GCT (teratoma, yolk sac, choriocarcinoma, mixed GCT)-normally affects 20-30yrs
Types of testicular cancer non-GCT?
sex cord/ stromal
Leydig, sertoli, lymphoma
What are the 4 stages of testicular cancer?
Stage 1- disease is confined to the testis
Stage 2- infradiaphragmatic nodes involved
Stage 3- supradiaphragmatic nodes involved
Stage 4- extralymphatic disease
