Renal and urology Flashcards
Define acute kidney injury (AKI)
Impairment of renal function over days or weeks, which often results in raised plasma urea/creatinine and oliguria (< 400 mL/day) and is usually reversible. The term acute kidney injury (AKI) represents the full spectrum of acute kidney dysfunction.
The resulting effects include impaired clearance and regulation of metabolic homeostasis, altered acid/base and electrolyte regulation, and impaired volume regulation.
Explain the aetiology / risk factors of acute kidney injury (AKI)
Risk factors:
Age >75, CKD, Cardiac failure, PVD, chronic liver disease, DM, drugs, sepsis, poor fluid intake/increased losses, urinary symptoms
Aetiology:
Commonest: ischaemia, sepsis and nephrotoxins (and prostatic disease)
- Pre-renal (40-70%)- reduced renal perfusion:
a. Hypovolaemic (acute haemorrhage, GI loss, renal loss (diuretics or osmotic diuresis), dermal loss (burns), sequestration of fluid (sepsis).
EXAMINATION: tachycardia, hypotension, reduced skin turgor, cold extremeties
b. Hypervolaemic, there is low effective circulating volume
(systolic heart failure–> cardiorenal syndrome, there are signs of HF; hypoalbuminaemia (decompensated liver disease)–> hepatorenal syndrome.
Renal artery obstruction- stenosis, embolism (see RAS below)
- Intrinsic renal (10-50%):
a. Tubular- acute tubular necrosis is most common cause of intrinsic renal AKI: ischaemia (from prerenal AKI), drugs (see below) and toxins (myoglobinuria in rhabdomyolysis), crystals (ethylene glycol poisoning, uric acid), and radiocontrast dye myeloma and raised Ca2+
b. Acute glomerulonephritis (see the condition)- autoimmune e.g SLE/HSP, drugs, infections, primary glomerulonephritides
c. Acute interstitial nephritis- drugs (see below), infiltration (lymphoma, infection, tumour lysis syndrome following chemo)
d. Small or large vessel osslusion: Renal artery/vein thrombosis, cholesterol emboli from angiography, vasculitis, malignant HTN, haemolytic microanipathy HUS/TTP, large vessel occlusion eg. dissection or thrombus
e. Other renal: Light chain (myeloma), urate (lympho- or myeloproliferative disorders, particaurlly after chemo/radiation induced cell lysis), pigment nephropathy (haemolysis/rhabdomyolysis, malaria), accelerated phase HTN (e.g. in pre-eclampsia)
3. Post renal (10-25%)- urinary tract occlusion. Most commonly due to BPH or prostate cancer in a male leading to frequent urination but slow urinary stream. Kidney stones stuck in ureter/urethra.
Luminal= stones, clots, sloughed papillae. Mural=malignancy, benign prostatic hyperplasia, strictures, blood clots, retroperitoneal fibrosis
Extrinsic compression=malignancy (esp. pelvic, prostate and bladder), retroperitoneal fibrosis
Summarise the epidemiology of acute kidney injury (AKI)
Epidemiology
Happens to 18% of hospital patients.
ATN counts for 45% of cases
Recognise the presenting symptoms of acute kidney injury (AKI)
(Rapid medicine:) Malaise, anorexia, nausea, vomiting, pruritus, drowsiness, convulsions, coma (caused by uraemia).
Recognise the signs of acute kidney injury (AKI) on physical examination
Palpable bladder, peripheral oedema, palpable kidneys (polycystic disease), abdo/pelvic masses, renal bruits, rashes
Identify appropriate investigations for acute kidney injury (AKI) and interpret the results
Outline the KDIGO staging for AKI
Blood: ABG, FBC, U&E (urea creatinine, Na+ and K+), LFT, ESR/CRP, Ca2+, clotting, culture, blood film: red cell fragmentation in HUS/TTP
Other BTs: CK (for rhabdomyolysis), urate, serum electrophoresis and autoantibodies
Urine: stick testing, haematuria, proteinuria (glomerulonephritis). Cukture and sensitivity, Bence-Jones protein (exclude myeloma.
Urine osmolality/Na+:
- Renal ARF: REDUCED urine osmolality (reduced urine concentrating ability), INCREASED urine Na+ (due to reduced resorptive ability), INCREASED fractional excretion of Na+ (PCr.UNa/PNa.UCr):>2%
- Pre-renal: i
Basic metabolic profile, ACR, urinalysis, urine culture, FBC, fractional excretion of sodium, fractional excretion of urea
KDIGO staging for AKI:
Stage 1: Increase serum creatinine 1.5x baseline in 48hr; urine output <0.5mL/kg/hr for >6 consec hours
Stage 2: Creatinine- increase 2-2.9 x baseline; urine output <0.5mL/kg/hr for >12 consec hours
Stage 3: Creatinine- increase >3 x baseline or commence RRT at any stage or urine output <0.3mL/kg/hr for >24hrs. Anuria (<100mLday)
Classified by whichever criteria puts them in the most severe stage of injury
Pre-renal AKI: bloods (urea and creatinine increased. Urea usually higher than creatinine) + urine (reduced urine outpout, reduced sodium and osmolalility)
Generate a management plan for acute kidney injury (AKI)
GENERAL:
Stop nephrotoxic drugs, stop metformin if creatinine greater than 150mmol/L
Aim for euvolaemia
Monitoring: aim for normal calorie intake (or more if catabolic, eg sepsis or burns) and protein 0.5g/kg/d. Consider nasogastric nutrition
Protect from hyperkalaemia by giving 10mL 10% calcium gluconate. IV insulin and dextrose to lower serum potassium if necessary, or salbutamol nebuliser, or IV sodium bicarb.
TREAT UNDERLYING CAUSE:
Pre-renal: correct hypovolaemia with fluids, sepsis with Abx
Post renal: catheterise and consider CTKUB… maybe cytoscopy and retrogade stends or nephrostomy
Instrinsic renal: refer to renal
RENAL REPLACEMENT THERAPY:
Haemodialysis (must be haemodynamically stable, and requires large-bore venous access e.g. internal jugular line. Usually done intermittently and good clearance of solutes)
Haemofiltration (often for ICU patients, much slower at clearing solutes, usually continuously performed)
Identify the possible complications of acute kidney injury (AKI) and its management
Hyperkalaemia, pulmonary oedema, uraemia (e.g. causing uraemic pericarditis - may require dialysis), acidaemia (may require dialysis)
Summarise the prognosis for patients with acute kidney injury (AKI)
Depends on early recognition and intervnetion
Can be as high as 80% mortality:
burns (80%), trauma/surgery (60%), medical illness (30%)
How do nephrotoxic drugs affect the kidney
Those causing acute tubular necrosis: paracetemol, aminoglycosides, amphotericin B, NSAIDs, ACEi and lithium
Those causing acute interstitial nephritis: NSAIDS, penicillins, thiazaide diuretics, sulphonamides, leptospirosis
How do burns affect the kidney
Reduce blood flow to them (even 20% of skin burns can do this)
Does BUN or creatinine increase more when GFR reduces, and why so?
BUN (=blood urea nitrogen)- because less is filtered AND because the filtrate moves more slowly though the PCT with reduced GFR, there is more time for BUN to be reabsorbed
Creatinine- only because less is filtered. Creatinine is not reabsorbed in the PCT, in fact it is actively secreted into the tubule in the DCT so the level of creatinine only increases due to reduced levels of filtration .
How can a BUN test be used to distinguish the cause of renal failure
In pre-renal renal failure, then the BUN will increase more than the creatinine (because BUN increases with reduced GFR due to less filtration and also more reabsorption, whereas creatinine just increases due to less filtration), so the BUN to creatinine ratio will INCREASE
In intrinsic renal failure, the BUN will only increase because less is being filtered out, NOT because it is being reabsorbed more. So the BUN will increase to the same extent as creatinine, so even though both values will increase, the ratio BUN: creatinine will stay the same.
Note that the normal BUN to creatinine ratio is between 10:1 and 20:1. Above this may mean there is not enough blood getting to the kidneys!
How can the urine osmolarity be useful to distinguish the cause of renal failure
In prerenal disease there is low perfusion of the kidneys resulting in reabsorption of Na+ and thus water, increasing the osmolarity of the kidneys (usually urine osmolairty above 500mOsm/kg suggests prerenal azotemia)
Typically, the Uosm in ATN is approximately 300 to 350 mOsm/kg, a value that is similar to the plasma osmolality (Posm) because the damaged tubules cannot reabsorb the Na+ and thus not absorb water. However, a Uosm of less than 500 mOsm/kg is often not diagnostically useful, because it can be seen in patients with ATN, prerenal disease, or underlying renal disease.
The SG of pre-renal renal failure also increases for this reason
Urine sodium concentration low in pre-renal failure too
Generally what factors can increase/decreased BUN and creatinine
Increase BUN: -Steroids, fever, GI bleeding, burns, Reduce BUN: -Liver failure Increase creatinine: -cimetidine and trimethoprim Reduce creatinine: -Having a small amount of muscle
What happens to sediment and FENa in pre-renal and renal AKI
Pre-renal: sediment -ve (unless progresses to ATN). FENa will be low because hardly any Na is excreted (kidney can reabsorb it), so usually <1%
Renal: sediment +ve due to dead cells. FENa higher because kidney cannot reabsorb the Na+, so usually >2%
What are the signs of ethylene glycol poisoning
confusion and dilated pupils
What might cause myoglobinuria
Recent crush injury
Signs in nephrotic syndrome and labs and somec causes
Signs: peripheral oedema, periorbital oedema, ascites
Labs: Proteinuria >3.5g/day Protein-to-creatinine ratio ?3g/g Hypoalbuminemia <3.5g/dL LDL >130mg/dL Triglyceride >150mg/dL. Lipiduria
Membranous nephropathy
Membranoproliferative glomerulonephritis
Signs in nephritic syndrome and labs and some causes
Signs: Arterial hypertension, peripheral edema
Labs:
Proteinuria 1-3g/day
5 dysmorphic RBCs/uL
Red cell casts
SLE Goodpastures disease (malaise, arthralgia, fever)
What is the most common cause of nephritic syndrome and how can it be investigated.
What are its signs
The most common cause of nephritic syndrome is poststreptococcal glomerulonephritis. It develops approximately 10 to 14 days after a group A beta-hemolytic streptococcal infection, most commonly of the upper respiratory tract but also of the skin.
Features of poststreptococcal glomerulonephritis include hematuria, edema, and hypertension. The condition is generally self-limited and resolves in a matter of weeks to months.
Anti-streptolysin O (ASO or ASLO) is the antibody made against streptolysin O, an immunogenic, oxygen-labile streptococcal hemolytic exotoxin produced by most strains of group A and many strains of groups C and G Streptococcus bacteria.
What are the signs of Immunoglobin A nephropathy
Immunoglobulin A nephropathy, or Berger’s disease, is the most common cause of glomerulonephritis worldwide (but note that the most common cause of nephritic syndrome is post-streptococcal glomerulonephritis) .
Asymptomatic, recurrent hematuria may occur 24~48hrs (not weeks, as in the case of ) following an upper respiratory infection or exercise.
Asymptomatic, recurrent hematuria may occur 24~48hrs (not weeks) following an upper respiratory infection or exercise. IgA levels may be elevated.
What is nephrotic syndrome
What constitutes proteinuria, and what about hypoalbuminaemia
A condition caused by damage to the glomeruli which makes them more permeable, and allows protein to escape.
The result is hypoalbuminaemia, proteinuria and peripheral and periorbital oedema
> 3.5g protein excreted per day
hypoalbuminaemia is <30g/L
..
…
What are those with nephrotic syndrome at risk of and why
- Clotting
Nephrotic syndrome patients are in a hypercoagulable state because they LOSE ANTITHROMBIN III from their urine too, which is the body’s anticoagulant
- Infection
Immunoglobulin proteins are also lost through the urine (in minimal change glumerulonpehritis, however, there is SELECTIVE loss of protein, just albumin not immunoglobulins)
What might happen to the urine in nephrotic syndrome and why
Frothy & foamy, because lipids are lost through the urine
What might you see in the urine under the microscope in nephrotic syndrome
Fatty casts (hyaline from dead epithelial cells that contained fat globules).
If these fatty casts are cholesterol rich, then the cholesterol would adopt a MALTESE CROSS appearance under polarized light (high yield!)
Given that lipids are lost in the urine in nephrotic syndrome, what happens to lipid levels in the blood
HYPERLIPIDAEMIA!
Liver increases lipoprotein production as a secondary change
Causes of nephrotic syndrome
Most common in children vs adults
Primary= Direct slcerosis of podocytes:
- Minimal change diseases
- Focal segmental glomerulosclerosis
- Membranous nephropathy
Secondary=Conditions not specific to kidney
- Diabetes (leads to nephrotic syndrome with Kimmelstiel-Wilson nodules)
- Sickle cell
- NSAIDs
- Lupus
- Sarcoid
- Multiple myeloma
- HIV
(it could be many conditions)
MOST COMMON CAUSES:
ADULTS: Focal segmental glomurulosclerosis (primary) Diabetes (secondary)
ELDERLY: Membranous nephropathy (do a chest X ray and breast examination to exclude malignancy)
CHILDREN: Minimal change glomerulonephritis (may have family history of atopy, most common SECONDARY cause of this condition is Hodgkins lymphoma)
What is the most common cause of nephrotic syndrome in kids?
What causes this disease and what is its effect in the glomerulus
Minimal change disease
Often idiopathic, triggered by recent infection, vaccination or immune stimulus (e.g. bee sting), but can be secondary to Hodgkin’s lymphoma
T cells in the blood release GPF (glomerular permeability factor) which damages the foot process of podocytes so they flatten out.
This is called EFFACEMENT
What is effacement and how does it contribute to nephrotic syndrome
Podocyte foot process effacement is present in most proteinuric diseases, such as MCNS, FSGS, membranous nephropathy, and IgA nephropathy (which is actually a nephritic syndrome)
It is considered to be a stereotypical reaction of podocytes to injury or damage.
T cells in the blood release GPF (glomerular permeability factor) which damages the foot process of podocytes so they flatten out.
The damaged foot processes lose their -vely charged coat, allowing -vely charged proteins like albumin to slip through into the
What are anti-GBM seen in. What are the pulmonary symptoms in this disease.
What othe system is affected and which symptoms
Goodpastures, which is an autoimmune, pulmonary-renal disorder. It affects collagen. (it’s a ANCA negative small vessel vasculitis)
Pulmonary symptoms include cough, shortness of breath, and hemoptysis.
Renal symptoms include hypertension, hematuria, and peripheral edema
Associated findings include glomerulonephritis and anti-glomerular basement membrane (GBM) antibodies.
Treatment for goodpastures
plasmapheresis (a method of removing blood plasma from the body by withdrawing blood, separating it into plasma and cells, and transfusing the cells back into the bloodstream. It is performed especially to remove antibodies in treating autoimmune conditions.)
immunosuppression
Define renal artery stenosis
Progressive narrowing of the renal artery
Explain the aetiology / risk factors of renal artery stenosis
What investigation would you do for the less common form, and what would you see
Atherosclerosis (80%)
Renal fibromuscular dysplasia (may be associated with micro-aneurysms in mid and distal renal arteries “string of beads on MR angiography”)
Decreased renal blood flow due to renal artery stenosis causes activation of the renin-angiotensin-aldosterone system, which in turn results in secondary hypertension.
Chronic renal hypoperfusion leads to hyperplasia of JGA to constantly secrete renin.
Renal hypoperfusion stimulates the renin-angiotensin system leading to increase circulating angiotensin II and aldosterone, increasing BP, which in turn, with time, causes fibrosis, glomerosclerosis and renal failure.
Summarise the epidemiology of renal artery stenosis
Prevalence is unknown but believed to account for 1– 5% of all hypertension; fibromuscular dysplasia occurs mainly in women with hypertension at < 45 years.
Recognise the presenting symptoms of renal artery stenosis
HTN REFRACTORY TO TREATMENT
Accelerated HTN and renal deterioration on starting ACEi
History of flash pulmonary oedema
History of HTN
Recognise the signs of renal artery stenosis on physical examination
Renal bruit may be heard
Hypertension that is often resistant to therapy
Features of renal insufficiency (e.g., nausea, edema)
Identify appropriate investigations for renal artery stenosis and interpret the results
What happens to kidney size? What would you class as significant RAS?
BLOODS:
- Creatinine: normal or raised
- Potassium: normal or low
- Urinalysis and sediment evaluation: normal in the absence of diabetic nephropathy or hypertensive glomerulosclerosis
- Aldo to renin ratio: Aldosterone-to-renin ratio <20 excludes primary aldosteronism as cause of hypertension and hypokalaemia or low-normal potassium
First imaging: Duplex ultrasound.
Sensitive only for lesions with >50% reduction in vessel diameter, and unable to provide further quantification of stenosis.
The gold standard for diagnosing renal artery stenosis is renal arteriography.
Findings:
Tubular stenosis of the proximal renal artery segment → typically atherosclerotic disease
Stenosis of the distal renal artery segment with a “string-of-beads” appearance → typically fibromuscular dysplasia
Significant renal artery stenosis: > 60% reduction in the diameter of the renal artery
Increased systolic flow velocity in the renal artery (Duplex)
Important, RAS should be suspected if:
-Hypokalemia in a newly diagnosed case of hypertension or
-An abrupt increase in creatinine after initiating ACE inhibitors or angiotensin receptor blockers
How does FENa help you distinguish the type of AKI
Simply, it compares the amount of sodium filtered out into the tubules with the amount that gets excreted.
In pre-renal AKI, most of the sodium which is filtered gets reabsorbed because the renin angiotensin system is activated, leading to sodium reabsorption. So the fraction of excreted sodium is LOW (less than 1%)
But in intrinsic AKI, there is impaired reabsorption of the sodium, meaning sodium is lost (as is water) into the urine. So the fraction of excreted sodium is HIGH (greater than 1%)
In post-renal AKI, the FENa will be less than 1% if the obstruction hasn’t damaged the tubules, and greater thna 1% if it has.
How does urine osmolality help you to distinguish the type of AKI
Similar to FENa.
In pre-renal AKI, the RAS is activated and there is effective reabsorption of sodium and water. So less water ends up in the urine, so you get high urine osmolality.
In intrinsic AKI, sodium (and thus water) isn’t effectively reabsorbed so there is usually a lower urine osmolality
In post-renal AKI, the osmolality will be high if the obstruction hasn’t damaged the tubules, and low if it has.
The main types of intrinsic AKI include
- Tubular (of which the most common is ACUTE TUBULAR NECROSIS)
- Interstitial (of which the most common is ACUTE INTERSTITIAL NEPHRITIS)
- Glomerular (of which the most common is GLOMERULONEPHRITIS
Match these 3 listed conditions to the following descriptions:
- Haematuria and proteinuria and dysmorphic RBCs and RBC casts
- Muddy brown granular epithelial cells casts on microscopy and renal epithelial tubular cells
- Eosinophilia on FBC and criteria , proteinuria and pyuria on dipstick, and microscopy there are white cells, white cell casts and RBCs
ACUTE TUBULAR NECROSIS:
-Muddy brown granular epithelial cells casts on microscopy and renal epithelial tubular cells
GLOMERULONEPHRITIS:
-Haematuria and proteinuria and dysmorphic RBCs and RBC casts
ACUTE INTERSTITIAL NEPHRITIS:
-Eosinophilia on FBC and haematuria, proteinuria and pyuria on dipstick, and microscopy there are white cells, white cell casts and RBCs
Define glomerulonephritis
.
Explain the aetiology / risk factors of glomerulonephritis
What are the possible presentation
Classify the causes, and match this to presentation
Different types with different aetiologies:
- Immune complex deposition forming within the glomerulus (more commmonly) or from the circulation.
- Non-inflammatory, metabolic processes (diabetes, amyloidosis).
It leads to damage to the glomerular filtration barrier
Most present with either
1) Isolated haematuria/proteinuria
2) Nephrotic syndrome
3) Nephritic syndrome
4) Acute renal failure
5) Chronic renal failure
Causes classified into PROLIFERATIVE and NON-PROLIFERATIVE
- Non-proliferative typically presents with NEPHROTIC syndrome
- Proliferative typically presents with NEPHRITIC syndrome
Give the 3 main conditions associated with proliferative and non-proliferative glomerulonephritis.
Give the main findings
NON-PROLIFERATIVE (–>nephrotic syndrome)
1) Minimal change glomerulonephritis
- 80% of all nephrotic syndrome in CHILDREN (20% of all nephrotic syndrome in adults)
- Can be ass. w tumours e.g. Hodgkin lymphoma
- Cause unknown
- URINALYSIS: SELECTIVE proteinuria (albumin gets through into urine but not immunoglobulins)
- LIGHT MICROSCOPY: no visible abnormalities
- IMMUNOFLUORESCENCE: no Ig or complement deposits
- ELECTRON MICROSCOPY: podocyte effacement, vacuolation and growth of microvilli on visceral epithelial cells.
2) Focal segmental glomerulosclerosis (FSGS)
- Most common cause of nephrotic syndrome in people of african/hispanic descent
- Ass with heroin abuse, HIV infection, obesity and sickle cell
- Hyalinosis (deposition of lipids and proteins in glomerulus)
- LIGHT MICROSCOPY: segmental sclerosis and hyalinosis
- IMMUNOFLUORESCENCE: often negative (as this is segmental) but SOMETIMES IgM and C3 in sclerotic regions
- ELECTRON MICROSCOPY: effacement of the foot processes
3) Membranous glomerulonephritis:
- Most common cause of nephrotic syndrome in white populations.
- PODOCYTES AND MESANGIAL CELLS DAMAGED (as opposed to just podocytes in membranoproliferative glomerulonephritis)
- Primary: anti-phospholipase A2 receptor antibodies
- Secondary: can be associated with infection (Hep B/C, malaria and syphilis), SLE, tumour and drugs (NSAIDS, penicillamine)
- SERUM: IgG antubodies against phospolipase A2 receptor
- LIGHT MICROSCOPY: glomerular capillary loops and BM thickening
- IMMUNOFLUORESCENCE: subepithelial granular deposits, diffuse uptake of IgG
- ELECTRON MICROSCOPY: subepithelial dense deposits “SPIKE AND DOME” appearance
These are also the primary causes of nephrotic syndrome. There are also secondary causes which you will see later
PROLIFERATIVE (nephritic syndrome):
1) IgA nephropathy (Berger’s)
- Typically presents as nephritic syndrome 24-48hrs following upper resp tract infection
- MOST COMMON TYPE OF GLOMERULONEPHRITIS IN ADULTS WORLDWIDE
- MICROSCOPY: increased numbers of mesangial cells, increased matrix
- IHC: IgA deposition IN THE MATRIX
2) Post streptococcal glomerulonephritis
- Presents 2 wees after infection with nephritic syndrome
- MICROSCOPY: diffuse proliferative and exudative glomerular histology, dominant C3 staining and subepithelial humps
- Raised streptotoccal titres
3) Membranoproliferative glomerulonephritis:
- Group of immune mediated disorders characterised histologically by GBM thickening and proligerative changes on light microscopy
- It should not be confused with membranous glomerulonephritis, a condition in which the basement membrane is thickened, but the mesangium is not.
- Associated with Hep C and some AI conditions e.g. SLE
Microscopy:
-thickened BM, thickened mesangium, “tram tracking appearance”
Immunofluorescence:
-Subendothelial deposition of IgG
Recognise the presenting symptoms of glomerulonephritis
-Differentiate nephrotic and nephritic syndrome
1) Nephritic syndrome
- haematuria, hypertension, oliguria, red cell casts and mild to moderate proteinuria
2) Nephrotic syndrome
- severe proteinuria, oedema, hypoalbuminaemia, hyperlipidemia and hypertension
Recognise the signs of glomerulonephritis on physical examination
.
Identify appropriate investigations for glomerulonephritis and interpret the results
.
Can you give a brief pathophysiology of nephritic syndrome, and 3 key diseases
NEPHRITIC:
- Inflammatory response within glomeruli leading to GBM disruption
1) Poststreptotoccal glomerulonephritis
2) IgA nephropathy
3) Goodpasture syndrome, Alport syndrome, microscopic polyangiitis
Can you give a brief pathophysiology of nephrotic syndrome, and 3 key diseases
NEPHROTIC:
- Structural damage of glomerular filtration barrier leading to massive renal loss of protein
1) Minimal change disease
2) Focal segmental glomerulosclerosis
3) Membranous nephropathy
4) Diabetic nephropathy
5) Amyloid light chain amyloidosis
What is henoch-schonlein purpura
What age groups is it common in
A type of IgA nephropathy affecting older children and presents with a triad of:
Abdominal pain
Arthritis
Purpuric rash
IgA nephropathy and HSP cause nephritic syndrome.
Common in kids <10
In all cases there is a rash of palpable purpura which are typically non-blanching. If there is no rash, then it is not HSP.
What are the lower urinary tract symptoms
FUN (storage problems i.e. can’t store, due to detrusor overactivity ):
- Frequency
- Urgency
- Nocturia
WISE (voiding problems, i.e. can’t void properly, due to obstruction of urethra):
- Weak stream
- Intermittency
- Straining
- incomplete Emptying
Terminal dribbling, urinary retention and overflow incontinence
Symptoms of prostate disease
LUTS (see the box above)
Symptoms of prostate cancer
LUTS
+
Metastasis (e.g. back pain due to bone mets)
+
Paraneoplastic syndromes (e.g. hypercalcaemia)
+
Constitutional upset (weight loss, malaise)
What should be used for symptomatic UTI in non-pregnenat women with uncomplicated UTI.
What about pregnant women
In non-pregnant women with uncomplicated UTI (normal urinary tract
structure and function), trimethoprim or nitrofurantoin are commonly used.
Alternative treatment options include co-amoxiclav or cephalexin.
Pregnant women
with UTIs require specialist attention because conventional treatment options (e.g.
trimethoprim, a folate antagonist) may cause harm to a foetus.
What would the serum osmolality look like in hyponatraemia secondary to SIADH
This is a euvolaemic hyponatraemia.
SIADH leads to increased retention of water causing
hyponatraemia and reduced serum osmolality. The urine is concentrated due to water reabsorption
Diabetic nephropathy can lead to nephrotic syndrome.
What happens to glomerular filtration rate
Pathology is characterized by an initial increase in glomerular filtration rate and glomerular basement membrane hypertrophy.
As the disease progresses, glomerulosclerosis occurs as a result of accumulation of extracellular matrix and destroying the filtering
ability of the glomerular membrane. This allows protein leakage.
First line management of nephrotic syndrome
Dietary measures to restrict sodium intake and a diuretic to control oedema
Albumin can be used as adjuncts in patients who are resistant to diuretic therapy but never in isolation.
What are the type of urinary tract stones by prevalence
Calcium oxalate – 75% Magnesium ammonium phosphate (struvite) – 15% Urate – 5% Hydroxyapatite – 5% Cysteine – 1%
Which side of the scrotum is more prone to varicocele
80-90% of varicocoeles occur on the left because of the angle at which the
left testicular vein meets the renal vein and increased reflux from compression of the
renal vein.
Describe the lumb from varicocele
Is it reducible?
Varicocoeles are usually asymptomatic, however, they can cause a sense
of scrotal heaviness. On examination, the lump is often described as feeling like a
‘bag of worms’.
Varicocoeles are reducible so the patient must be standing when
examined and actions that increase intra-abdominal pressure (e.g. Valsalva
manoeuvre, coughing) can increase the dilatation.
T/F varicoceles are associated with infertility
T
How is the lump if it’s a hydrocele
It would not be possible to
distinguish the swelling from the testicle in a hydrocoele.
How is the lump if it’s an epididymal cyst
Epididymal cysts will not
reduce when lying down and it would cause a smooth, fluctuant swelling rather than
a ‘bag of worms’ (which is the case in varicocele)
What causes the purpuric rash in HSP
Immune complexes are
deposited in the skin, mucous membranes, joints and organs.
Define benign prostatic hyperplasia
Slow progressive NODULAR hyperplasia or the TRANSITIONAL zone of the prostate gland.
Most common cause of LUTS in adult males
Explain the aetiology / risk factors of benign prostatic hyperplasia
What area of the prostate is typically affected in BPH vs prostate cancer. How does this affect onset of LUTS
RFs: Related to age, testosterone and dihydrotestosterone exposure, obesity, diabetes, dyslipidaemia, genetic, afro-caribbean
Epithelial and stroma hyperplasia of transition zone of the prostate. This then becomes surrounded by a false capsule of compressed peripheral zone glandular tissue.
BPH: transitional zones, which is closer to the urethra than,
PROSTATE CANCER: which occurs usually in the peripheral zone, which is further away from the urethra and thus presents with LUTS much later than BPH does
Summarise the epidemiology of benign prostatic hyperplasia
70% of men aged 70 have histological BPH, with 50% of those experiencing significant symptoms
Recognise the presenting symptoms of benign prostatic hyperplasia
LUTS are separated into storage problems and voiding problems.
Voiding (obstructive) problems:
-Hesitancy, poor stream, terminal dribbling, incomplete empyting
Storage problem (destrusor contracting too much):
- Frequency
- Urgency
- Nocturia.
Acute retention: sudden inability to pass urine, associated with severe pain
Chronic retention: painless, frequency with passage of small volumes of urine, especially at night
Recognise the signs of benign prostatic hyperplasia on physical examination
DRE: prostate is enlarged. Poor correlation between size and symptoms.
If NODULAR on DRE, prostate carcinoma should be suspected
Acute retention:
suprapublic pain and distended bladder
Chronic retention:
large distended painless bladder (residual volumes >1L), may be signs of renal failure
Identify appropriate investigations for benign prostatic hyperplasia and interpret the results
Bloods:
U&E (renal function,
PSA
Urine:
MCS
Imaging:
Ultrasound imaging of renal tract to check for dilation of upper urinary tract. Bladder scanning to measure pre- and postvoiding volumes
Transrectal ultrasound:
To measure prostate size and guided biopsies
Histology:
Epithelial and stromal hyerplasia of the transitional zones, becomes surrounded by false calsule in the peripheral zone
Flexible cystoscopy:
To visualise bladder outlet and bladder changes (trabeculation)
Other
Urinary flow studies
Generate a management plan for benign prostatic hyperplasia
Acute retention
BPH without acute retention
Acute retention:
-Urinary catheterisation
Otherwise….
Conservative:
-Watchful waiting with symptom monitoring using questionnarie
-Reduce evening fluid intake
Medical:
- Selective a-blockers to relax smooth muscle of the internal sphincter and the prostate capsule (alfuzosin, samsulosin). Works within 24-48hrs.
- 5 a-reductase inhibitors act to inhibit conversion of testosterone to dihydrotestosterone (finasteride). These reduce prostate size by 20% but may tale time. Takes 3-6 months.
Surgical:
- Transurethral resection of the prostae (TURP)
- Resection from within prostatic urethra, using electrocautery, laser.
- Open prostatectomy (for VERY large glands, >60g)
Identify the possible complications of benign prostatic hyperplasia and its management
Recurrent UTIs, acute or chronic retention, urinary stasis and bladder divertivuale or stone development. Obstructive renal failure, post obstructive diuresis
FROM TURP:
-Retrograde ejaculation (common)
- Haemorrhage (primary, reactionary of secondary)
- Clot retention
- Incontinence, TUR syndrome (seizures or cardiovascular collapse caused by hypervolaemia and hyponatraemia due to absorption of glycine irrigation fluid)
- Urinary infection
- Erectile dysfunction
- URETHRAL STRICTURE
Summarise the prognosis for patients with benign prostatic hyperplasia
Mild symptoms may be improved by medical therapies
Marked symptoms usually relieved from surgical intervention
What is BPE vs BPH
BPE is the clinical finding of an enlarged prostate due to the histological process of benign prostatic hyperplasia
BPH is a histological basis of a diagnosis of benign prostatic enlargement resulting in bladder outflow obstruction
What is bladder outlet obstruction
bladder outlet obstruction caused by benign prostate enlargement
How can DRE be relevant to treatmnet
A large prostate may benefit from alpha reductase inhibitors.
Small ones won’t
What counts as obstructed blow
Less than 12mL/S
Overactive bladder treatment
CONSERVATIVE:
- Reassure and treat triggering UTI
- Dietary advice
- Bladder retraining
MEDICAL:
-Anticholindergics (cause dry eye, dry mouth, serious cause glaucoma)
-Beta agonist (CI in HTN)
SURGICAL:
-Intravesical botox injection
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Define testicular cancer
Malignancy arising in testes
