Renal & Urology Overview Flashcards
What are the functions of the kidney?
- regulation of blood pressure & volume via RAAS
- acid-base balance
- electrolyte balance
- production of new RBCs stimulated by Epo
- contains 1-alpha-hydroxylase, which is needed to produce the active form of vitamin D
- acts as a filter for the excretion of water-soluble waste products
How is the kidney involved in bone metabolism?
- the prohormone, 25(OH)D is produced in the liver
- the kidney contains 1-alpha-hydroxylase, which will hydroxylate the prohormone to produce the active hormone
- active vitamin D leads to increased calcium absorption in the gut and the bone
How is renal function measured?
renal function = flow rate from the glomerulus into the Bowman’s capsule
- this is the glomerular filtration rate (GFR)
- it is a measure of the volume of blood being filtered by the glomerulus each minute
- any value of GFR > 90 ml/min is considered normal
- this means that the glomerulus is filtering 90ml of blood each minute
- GFR typically reduces at a rate of 1 ml/min/year
What is the gold standard measurement of GFR?
- the only way that GFR can be measured is with inulin clearance
- inulin is freely filtered by the glomerulus, not secreted or reabsorbed in the tubules and is not synthesised or metabolised by the kidney
- calculations involve concentrations of inulin in the urine and serum
How can blood urea be used as an endogenous marker of GFR?
- urea is a by-product of protein metabolism that is freely filtered at the glomerulus
- it has variable reabsorption (30-60%) depending on nutritional state, hepatic function and GI bleeding
- e.g. GI bleed can raise serum urea
- raised serum urea can indicate poor kidney function
How can serum creatinine be used to estimate GFR (eGFR)?
What equation is used to work this out and what factors does it take into account?
- creatinine is derived from muscle cells, freely filtered at the glomerulus and not reabsorbed
- the Cockcroft-Gault equation is used to estimate creatinine clearance and eGFR
- this estimates how much creatinine is being cleared from the blood
- creatinine clearance is affected by age, sex, ethnicity and weight
- more creatinine is produced when there is more muscle mass
What would a normal urea : creatinine ratio be?
- urea is reabsorbed by the tubules, but creatinine is not
- normal urea to creatinine ratio is 40:1 to 100:1
- this ratio is used when looking at different types of kidney injury
What is the problem with the Cockroft-Gault equation?
- it is used to measure creatinine clearance as a measure of eGFR
- it often overestimates the true GFR, especially when < 30 ml/min
If both of these people have a serum creatinine of 100, why is it important to measure eGFR?
- creatinine clearance (eGFR) is important to measure when giving drugs that are renally cleared
- if the drugs are not being cleared sufficiently, it can lead to renal toxicity
500ml of 0.9% saline over 15 minutes
- this looks like a pre-renal AKI
- need to give an IV fluid bolus and maintenance fluids
-
hold nephrotoxic medications
- metformin
- NSAIDs
- ACE-inhibitors
What mnemonic can be used to remember the nephrotoxic drugs?
DAMN
- D - diuretics
- A - ACEi / ARBs
- M - metformin (can predispose to lactic acidosis)
- N - NSAIDs
What is meant by acute kidney injury?
Why does it occur and how is it measured?
- a rapid decline in renal function over hours to days
there is failure to maintain homeostasis of:
- fluid - leading to oliguria** or **volume overload
- electrolytes - leading to hyperkalaemia
- acid-base balance - leading to metabolic acidosis
- it is measured by looking at urea and creatinine
What are 2 easy ways to spot an AKI?
Is it reversible?
- the easiest way to recognise AKI is that the patient stops peeing
- look at creatinine** as this will be **acutely raised
- it is potentially reversible
What is meant by chronic kidney disease?
How is it diagnosed?
- this is a chronic and irreversible process with 5 stages
- there must be impaired renal function for > 3 months based on:
- abnormal structure or function
- or GFR < 60 ml/min for > 3 months
- +/- evidence of kidney damage
- this is progressive and irreversible, ending in end-stage renal failure
- it is monitored by looking at eGFR
What symptoms may someone with an AKI present with?
symptoms depend on underlying cause, but typically:
-
oliguria / anuria
- abrupt anuria suggests a post-renal cause
- nausea & vomiting
- dehydration
- shortness of breath
-
confusion
- encephalopathy from uraemia (build-up of urea in the brain)
What signs might someone with AKI present with?
- hypertension
-
distended bladder
- typically seen with an obstructive cause
- postural hypotension due to dehydration
- if they have fluid overload - raised JVP, peripheral / pulmonary oedema
- i.e. in cirrhosis, heart failure, nephrotic syndrome
- if they have vascular disease - bruising, rash, pallor
What classification system is used for AKI?
KDIGO classification system
- need to check the patient’s baseline creatinine to determine whether a rise is significant
Stage 1:
- 1.5x rise in creatinine compared to baseline
- OR urine output <0.5 ml/kg/hr for > 6 hours
Stage 2:
- 2x rise in creatinine compared to baseline
- OR urine output <0.5 ml/kg/hr for > 12 hours
Stage 3:
- 3x rise in creatinine compared to baseline
- OR urine output < 0.3 ml/kg/hr for > 24 hours
- OR anuria for > 12 hours
What are the risk factors for AKI?
What mnemonic can be used?
CHARD CH
- C - chronic kidney disease
- H - hypovolaemia
- this is the most common cause of AKI
- A - age > 75
- R - renal transplant
- D - diabetes
- C - contrast administration
- H - heart ailure
What is meant by a pre-renal cause of AKI?
What 4 states can lead to pre-renal AKI?
there is inadequate perfusion to the kidney
when there is decreased blood flow to the glomerulus, there is decreased blood filtration
- this is most commonly due to hypovolaemia
- systemic vasodilatation (e.g. in sepsis)
- decreased cardiac output
- intrarenal vasoconstriction
What is meant by renal and extrarenal losses leading to hypovolaemia and pre-renal AKI?
Renal loss:
- loss of fluid from diuretic overuse
- osmotic diuresis (e.g. diabetic ketoacidosis)
Extrarenal loss:
- vomiting and/or diarrhoea
- burns
- sweating
- blood loss
What can cause systemic vasodilatation or decreased cardiac output leading to pre-renal AKI?
Systemic vasodilatation:
- sepsis
- neurogenic shock
Decreased cardiac output:
- heart failure
- myocardial infarction
What can cause intra-renal vasoconstriction leading to pre-renal AKI?
- cardiorenal syndrome
- hepatorenal syndrome
- renal artery stenosis
What are the consequences of pre-renal AKI?
What will happen to the urea:creatinine ratio and why?
-
reduced urine output
- if there is no bloodflow to the kidney, urine cannot be produced
- urea is raised much higher than creatinine so urea:creatinine > 100:1
- this is due to dehydration and urea resabsorption by the kidneys
- urea is still being reabsorbed as the kidneys themselves are not damaged
What is involved in the inital management of pre-renal AKI?
What factors need to be monitored?
- start with NEWS monitoring and observe for life-threatening complication
- should be able to identify hyperkalaemia / hypovolaemia
- need to treat hypovolaemia
- catheterise the patient to monitor fluid balance
- need to monitor K+, lactate (for signs of sepsis) and daily creatinine
What is involved in investigations for pre-renal AKI?
Urine dipstick:
- proteinuria and/or haematuria could be a sign of glomerulonephritis
USS:
- should be performed within 24 hours unless there is an obvious cause
VBG:
- check electrolytes, glucose & lactate
- check platelets to rule out thrombotic cause like HUS or TTP
- if AKI does not improve, consider investigations for intrinsic renal disease
What is involved in the management of pre-renal AKI?
- bolus fluid and maintenance fluid
- treat the underlying cause e.g. sepsis
- stop nephrotoxic medications
-
stop / change medications that are heavily renally excreted
- e.g. LMWH
- if eGFR < 30 then use another form of prophylactic VTE
- avoid radiological contrast
Which class of antibiotics are known to be nephrotoxic?
aminoglycosides
(e.g. amikacin, gentamicin)
these can cause acute tubular necrosis
What causes a renal AKI?
What are the 4 different types?
- this is caused by cellular / intrinsic damage to the kidney
- the different types depend on where the damage is located
- tubular
- glomerular
- interstitial
- vascular
What is the main tubular cause of renal AKI?
What causes this?
acute tubular necrosis
- ischaemia
-
drugs
- NSAIDs
- paracetamol
- ACE inhibitors
-
toxins
- contrast
- myoglobulinuria in rhabdomyolysis
- these cause death of the tubular epithelial cells than form the renal tubules of the kidneys
How are the renal tubular epithelial cells damaged in acute tubular necrosis?
-
prolonged hypoperfusion state leading to ischaemia
- this can be due to pre-renal AKI from sepsis that has not been treated and has progressed
- systemic vasodilation - sepsis, DIC
- exogenous and endogenous nephrotoxic agents
How does acute tubular necrosis cause AKI?
- death of renal tubular epithelial cells leads to sloughing of these cells and obstruction of the tubules
- there is increased hydrostatic pressure within the tubules, which leads to reduced GFR
- there is reduced filtration / reabsorption
- this leads to reduced urine output
What are exogenous and endogenous nephrotoxins that can cause ATN?
Exogenous (drugs):
- aminoglycosides
- NSAIDs
- contrast media
- cisplatin
- calcineurin inhibitors
- amphotericin B
Endogenous:
- myoglobinaemia (rhabdomyolysis)
- haemoglobinuria
- uric acid crystals
- IgG light chains in myeloma
What urine findings would you expect to see in ATN?
- muddy brown granular casts of epithelial cells
- myoglobinuria and haemoglobinuria
What features of renal AKI would you expect to see in ATN?
How would urea : creatinine be affected?
- raised urea
- raised creatinine
- raised potassium
- metabolic acidosis
- in renal causes of AKI, urea : creatinine is < 40 : 1
- the kidney itself is not functioning, so urea cannot be reabsorbed
Hyperkalaemia is a complication of renal AKI.
What is involved in the management of this condition?
- medical emergency so escalate senior help and start ABCDE approach
- hyperkalaemia carries risk of cardiac arrhythmias + cardiac arrest
- continuous cardiac monitoring + baseline ECG + IV access
- stop any nephrotoxic drugs
- give 10ml 10% calcium gluconate** IV over **10 mins
- this protects the myocardium but onset is 4 hours
- give 100ml 20% dextrose** with **8U insulin** over **15 mins
- give 10-15mg nebulised salbutamol
- sodium bicarbonate 1.26% over 6 hours to correct acidosis
- monitor ECG changes
- (insulin and salbutamol both work to drive K+ back into cells and out of the blood)*
What ECG changes are associated with hyperkalaemia?
- tall tented T waves
- small / absent P waves
- broad QRS complex
- increased PR interval
- bradycardia
- VT
What is the main cause of glomerular renal AKI?
glomerulonephritis
- this is inflammation of the glomeruli and nephrons
- there are many different types of glomerulonephritis with different aetiologies
- e.g. postinfectious
How does glomerulonephritis show up on urine dipstick and BP?
- blood pressure can range from normal to malignant hypertension
- proteinuria and haematuria will be present on urine dipstick
What are the consequences of glomerular inflammation on renal function?
How do these present?
Loss of barrier function:
- when podocytes are damaged and the barrier is lost, there is loss of protein and blood
- proteinuria (mild to nephrotic syndrome)
- haematuria (mild to macrocytic)
Loss of filtering capacity:
- reduced excretion leads to accumulation of waste products and AKI
What is the interstitial cause of renal AKI?
interstitial nephritis
- this is caused by drugs, infection and infiltration
- it involves inflammation of the renal interstitium (fluid surrounding the renal tubules)
- there will be eosinophils in the urine
What are the vascular causes of renal AKI?
- this is caused by vessel obstruction
- thrombosis
- vasculitis
- haemolytic microangiopathy
In order to make urine, how many layers do the solutes have to pass through?
- blood enters glomerulus via an afferent arteriole
- within the glomerulus, solutes must then pass through the wall of the Bowman’s capsule
- endothelial cells
- glomerular basement membrane
- slit diaphragms of podocytes
- solutes (urea, electrolytes, waste products) are then within the urinary space
- they will then pass into the renal tubules that lead to the collecting ducts
What is meant by acute pyelonephrititis?
- inflammation of the renal pelvis of the kidney
- it is a form of upper urinary tract infection that is usually caused by bacteria
What is the difference between a lower and an upper urinary tract infection?
- a lower UTI affects the urethra and the bladder
- an upper UTI affects the ureters and the kidneys
- an upper UTI is usually caused by ascending infection
- bacteria begin by colonising the urethra / bladder and then make their way up the ureter to the kidney
What are the risk factors for an upper UTI?
the risk factors for upper UTI are very similar to those of a lower UTI
- female sex
- sexual intercourse
- indwelling catheter
- diabetes
- urinary tract obstruction
- vesicoureteral reflux (VUR)
What is meant by vesicoureteral reflux (VUR)?
Why does it happen?
- urine can move backwards up the urinary tract
- this occurs when the vesicoureteral orifice fails
- this is a one way valve that allows urine to flow from each ureter into the bladder
- this can be due to a primary congenital defect
- OR it can be due to bladder outlet obstruction
- this leads to increased pressure within the bladder, which distorts the valve
Why is someone with vesicoureteral reflux more likely to get acute pyelonephritis?
- when there is a bladder outlet obstruction, there is also urinary stasis
- this makes it easier for bacteria to adhere to and colonise the urinary tract
- bacteria can ascend from the bladder, up the ureters and into the renal pelvis
Other than ascending infection, how else may the renal pelvis become infected to cause acute pyelonephritis?
Which organisms are associated with this method of transmission?
- kidneys can be infected via haematogenous spread
- this is the spread of infection via the bloodstream
- pyelonephritis from haematogenous spread is usually a complication of sepsis, bacteraemia or infective endocarditis
- this is most commonly due to E. coli or Staphylococcus spp.
What might be found in the urine of someone with acute pyelonephritis?
Why does this occur?
white blood cells in urine + white blood cell casts
- bacteria start adhering to the renal epithelium, which triggers an inflammatory response
- cytokines attract neutrophils to the renal interstitium
- neutrophils infiltrate and die off
- dead neutrophils pass through the urinary tract and are excreted in the urine
- cells and protein debris may be cast into the shape of the tubule and then excreted - this is cast
What triad of symptoms is associated with acute pyelonephritis?
What condition is it difficult to distinguish from?
- it is difficult to clinically distinguish from a lower UTI
- the triad of:
- flank pain (usually unilateral) at the costovertebral angle
- nausea & vomiting
- fever
occurs more often in acute pyelonephritits than lower UTI
- onset is typically sudden with signs and symptoms of both systemic inflammation and bladder inflammation
What is meant by chronic pyelonephritis?
- chronic inflammation of the renal pelvis and kidney
- usually caused by recurrent episodes of acute pyelonephritis, which leads to the kidney becoming visibly scarred
What is the most common risk factor for having recurrent episodes of acute pyelonephritis that progresses to chronic pyelonephritis?
vesicoureteric reflux (VUR)
- urine flows backwards up the urinary tract due to failure of the vesicoureteric orifice
- this occurs due to a primary congenital malformation
- or due to bladder outlet obstruction, which increases the pressure within the bladder and distorts the valve
What is meant by unilateral obstruction?
Will this affect one or both kidneys?
- this is an obstruction higher up in the urinary tract (e.g. ureters)
- this will only affect one kidney
- the most common cause of unilateral obstruction is renal calculi (kidney stones)
What changes occur in the kidney when there is recurrent inflammation?
Which parts of the kidney tend to be affected?
- one episode of inflammation may not lead to any permanent damage
- recurrent inflammation eventually leads to fibrosis and scarring of the renal interstitium
- renal tubules will atrophy
- these changes tend to be found in the upper and lower poles of the kidney
What would be seen on imaging in chronic pyelonephritis?
- CT urogram shows blunting / flattening of the renal calyces
What is seen on histology in chronic pyelonephritis?
- some tubules may be dilated and full of glassy-looking proteinaceous material called colloid
- colloid forms as a result of chronic inflammation
- it ends up becoming shaped like the tubules and forming colloid casts** that are **excreted in the urine
- this is sometimes called “thyroidisation of the kidney” as the colloid resembles thyroid tissue
What happens in xanthogranulomatous pyelonephritis (XGP)?
- this is a rare form of chronic pyelonephritis
- it occurs when an infected kidney stone causes a chronic obstruction
- the combination of infection and increased pressure creates granulomatous tissue
- there is destruction of the renal parenchyma, which is replaced with granulomatous tissue
How can xanthogranulomatous pyelonephritis be recognised on histology?
the presence of granulomatous tissue
- this is full of foamy (fat-laden) macrophages
- it is easily confused for a kidney tumour on imaging
What type of infection and kidney stone is associated with development of xanthogranulmoatous pyelonephritis (XGP)?
- staghorn kidney stone is large and branching in nature
- it is associated with _*Proteus* infections_
- Proteus bacteria will alkalinise the urine, leading to an ammonia smell
- chronic Proteus infections are associated with XGP, which presents with necrotic, haemorrhagic masses with foamy macrophages
What is cystitis?
What different things can cause it?
- cystitis is a lower UTI that involves inflammation of the bladder
- it is usually due to bacterial infection, but can also be caused by:
- fungal infection
- trauma to the bladder
- chemical irritation
- foreign bodies (e.g. kidney stone)
What is meant by an ascending and descending infection?
Which is more common in cystitis?
- lower UTIs are nearly always caused by ascending infection
Ascending infection:
- bacteria migrate from the rectal area** to the **urethra
- they then migrate up the urethra and into the bladder
Descending infection:
- bacteria start in the blood or lymph
- this is most commonly pyelonephritis as a consequence of sepsis/bacteraemia
- they infect the kidneys and then descend down the ureters and into the bladder and urethra
What is meant by urine being sterile?
What 2 mechanisms are in place to prevent bacteria from growing in the urine?
- normally urine is sterile and contains NO bacteria
- urine is high in urea** and has a **low pH which helps to stop bacterial growth
- the unidirectional flow when urinating helps prevent bacteria invading the urethra and bladder
Which Gram-negative and Gram-positive bacteria commonly cause cystitis?
Gram-negative:
-
Escherichia coli
- this is the most common cause of lower UTI
- Proteus mirabilis
- Klebsiella pneumoniae
- Enterobacter spp. and Citrobacter spp.
Gram positive:
-
Staphylococcus saprophyticus
- this is the 2nd most common cause of lower UTI
- it is more prevalent in sexually active young females
- Enterococcus spp.
Why does being female increase the risk of cystitis?
- females have a shorter urethra
- this means that bacteria ascending up the urethra do not have to travel as far
- the urethra is also closer to the rectum, which is where most of the causative organisms originate from
- in post-menopausal women, a decrease in oestrogen leads to the loss of the normal protective vaginal flora, increasing risk of UTI
How does diabetes mellitus act as a risk factor for cystitis?
- diabetes is a risk factor due to the presence of hyperglycaemia
- normally, when there is an infection, neutrophils move out of the circulatory system (blood) towards the infection in the process of diapedesis
- neutrophils also carry out phagocytosis
hyperglycaemia inhibits diapedesis and phagocytosis
- this means that neutrophils are less effective at killing bacteria
What are the typical symptoms of cystitis?
- suprapubic pain
-
dysuria
- this is pain on urinating / difficulty urinating
- frequent urination
- increased urgency
If you dipstick the urine of someone with cystitis, what would you expect to see and why?
Leukocyte esterase:
- this is an enzyme produced by WBCs that is positive in pyuria
Nitrites:
-
gram-negative bacteria convert nitrates into nitrites
- nitrities will not always be positive in UTI
- associated with E. coli, Klebsiella & Proteus
What is sterile pyuria?
What does it suggest if this is present?
- this occurs when there is pyuria** but **urine culture is negative
- as there is pyuria, leukocyte esterase will be positive
- this suggests urethritis (inflammation of the urethra)
- this is commonly caused by Neisseria gonorrhoeae and Chlamydia trachomatis
- these are both sexually transmitted infections
- urethritis presents with the same symptoms as cystitis so this is used to distinguish between them
What 3 imaging techniques may be used in cystitis?
Renal ultrasound:
- used in children to identify kidney malformations
Voiding cystourethrogram (VCUG):
- this involves injection of radiocontrast fluid and watching how it moves when urinating
- this can be used to detect vesicoureteral reflux (VUR)
Renal scintigraphy:
- involves injection of DMSA and detecting evidence of renal scarring
What is the normal flow of urine like?
- urine is produced by the nephrons
- it passes through the renal papillae and into the calyces
- from the calyces it enters the renal pelvis, which drains into the ureter
Why does hydronephrosis occur?
What are the 2 main categories of causes?
- it occurs when there is an obstruction to the normal flow of urine
- this increases pressure within the urinary system and causes the walls of the structures involved to dilate
- this can occur due to internal causes - i.e. an obstruction within the urinary tract
- e.g. kidney stones
- or it can occur due to external compression
- e.g. foetus compressing the urinary tract in pregnancy
What are the 2 most likely causes of hydronephrosis in a young child?
the cause is likely to be congenital
-
ureterocoele
- this is a sac of tissue in the distal ureter that obstructs the flow of urine into the bladder
-
posterior urethral valves
- these are flaps of tissue that obstruct the outflow of urine
What damage can long-standing hydronephrosis lead to?
- long-standing hydronephrosis can lead to nephron destruction
- this leads to a rise in serum creatinine and electrolyte disturbances
- continued damage can cause dilated ureter and renal pelvis
- as well as compression atrophy** - this is **thinning of the renal cortex and medulla
What is meant by benign prostatic hyperplasia (BPH)?
- this is the non-cancerous growth of the prostate gland
- hyperplasia means increase in the number of cells
- benign (non-cancerous) means that they do not invade into neighbouring tissues
- it is common in men > 50 and is considered a normal part of aging
Where is the prostate located?
Which structure passes through it?
- it is a small gland about the size of a walnut
- it is located inferior to the bladder and anterior to the rectum
- the urethra passes through the prostate gland before reaching the penis
- this part of the urethra is known as the prostatic urethra
What are the 3 zones of the prostate?
What are they surrounded by and what do they contain?
- the prostate is surrounded by a capsule of tough connective tissue and smooth muscle
Peripheral zone:
- this is the largest zone and is the outermost posterior section
- it contains 70% of the glandular tissue
Central zone:
- it contains 25% of the glandular tissue and the ejaculatory ducts that join with the prostatic urethra
Transitional zone:
- it contains 5% of the glandular tissue and the prostatic urethra
- contains transitional cells that are also found in the bladder
What types of cells are found within the basement membrane that surrounds the tiny prostate glands?
- each of the tiny glands that make up the prostate is surrounded by a basement membrane
- within this basement membrane is a layer of cube-shaped basal cells
- neuroendocrine cells are interspersed between the basal cells
- there is a row of luminal columnar cells within the lumen / centre of the gland
What is secreted by the luminal cells of the prostate?
- they secrete substances into the prostatic fluid which make it slightly alkaline
- they also give nutrients into the prostatic fluid which nourish the sperm and help them to survive in the acidic environment of the vagina
What is involved in the process of ejaculation?
Where do sperm, semen and prostatic fluid join together?
- during an ejaculation, sperm leave the testes and travel through the vas deferens into the ejaculatory ducts
- the ejaculatory ducts** join with the **prostatic urethra
- smooth muscle within the prostate contracts to push prostatic fluid into the urethra
- here it joins with the sperm and semen (from seminal vesicles)
What hormones do the basal and luminal cells of the prostate rely on for survival?
Where do these hormones come from and how do they exert an effect?
- basal and luminal cells rely on stimulation from androgens
- testosterone is produced in the testes
- dihydrotestosterone is produced within the prostate gland
- androgens are steroid hormones so they can cross the cell membrane and bind to androgen receptors in the nucleus
- this process inhibits apoptosis, which allows the basal and luminal cells in the prostate to keep growing and multiplying
How does dihydrotestosterone differ from testosterone?
How is it produced?
- it is produced in the prostate by 5a-reductase
- 5a-reductase converts testosterone into dihydrotestosterone
- dihydrotestosterone is 10x more potent than testosterone as it can bind to androgen receptors for longer
What happens to the levels of testosterone and dihydrotestosterone with increasing age?
- after the age of 30 men produce 1% less testosterone per year
- the amount of testosterone decreases with age
- 5a-reductase activity increases with age
- there is an increase in levels of dihydrotestosterone
- normal prostate cells respond to the increase in dihydrotestosterone by living longer and multiplying
- this leads to an increase in the size of the prostate gland
Where do hyperplastic nodules tend to form within the prostate?
How can this lead to effects on the bladder?
- hyperplastic nodules tend to form in the periurethral zone
- this is the area surrounding the prostatic urethra
- nodules can compress the urethra and make it more difficult for urine to pass through
- urine builds up in the bladder and causes it to dilate
- smooth muscle in the bladder wall contracts harder in response
- this leads to bladder hypertrophy - the walls thicken and become easily irritated
- stagnation of urine in the bladder also promotes bacterial growth and can lead to UTIs
How can BPH be diagnosed?
What blood test may be performed?
through digital rectal examination (DRE)
- the anterior wall of the rectum lies along the posterior prostate
- an enlarged prostate could indicate BPH, whilst hard nodules could be a sign of prostate cancer
-
levels of PSA are elevated in BPH
- this is produced by healthy prostate cells
- there is an increase in number of prostate cells in BPH
