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
Explain the aetiology / risk factors of testicular cancer
Testicular maldescent (cryptorchidism) or ectopic testis increases risk by 40x.
Others risk factors:
- Contralateral tesicular tumour
- Family history
- Mumps
- Maternal oestrogen exposure
GERM CELL (commoner-95%)
1) SEMINOMAS (40%, peak 30-40)
2) NONSEMINOMATOUS GERM CELL TUMOURS (60%, peak in 20-30 years).
- Embryonal cell caricinoma
- Choriocarcinoma
- Yolk sack tumours
- Teratomas.
NON-GERM CELL (rarer)
- Sertoli and Leydig cell tumours
- Non-hodkins lymphoma.
Summarise the epidemiology of testicular cancer
Uncommon.
1% of male malignancy
BUT
Most common malignancy in 18-35 years
Trimodal peak incidence: infancy, 25-40 years and 50 years.
Caucasians at higher risk
Recognise the presenting symptoms of testicular cancer
Testicular lump noticed.
Rarely:
Backache due to para-aortic lymphadenopathy or
Signs of lung mets
Recognise the signs of testicular cancer on physical examination
Differentiate the appearance of seminomas and teratomas
Painless hard testicular mass (may be secondary hydrocele)
Lymphadenopathy (supraclavicular, para-aortic)
Signs of pleural effusion
Gynaecomastia (resulting from hCG production)
Seminomas are pale, cream-white, solid and well circumscribed
Teratomas are cystic in appearance with haemorrhagic and necrotic areas
Identify appropriate investigations for testicular cancer and interpret the results
Bloods:
Tumour markers a-fetoprotein, b-HCG, LDH
Urine: Pregnancy test (positive if the tumour produced b-HCG!)
Testicular ulstrasound:
View primary tumour
Staging:
CT abdomen, chest, brain if extensive disease
MRI in equivocal lesions or FDG-PET to evaluate residual sminoma masses.
TNM or Royal Marsden staging: I- limited to testis II- abdominal lymphadenopathy; A-<2cm, B-2.5cm, C->5cm. III-nodal involvement above diaphragm (ABC as above) IV-extra-lymphatic metastases
Immediate investigations in suspected testicular cancer
Bloods- FBCs, U&Es, tumour markers
USS testes
Chest x-ray (lung mets may be seen)
Tumour markers must be measured before orchidectomy or chemo
Which tumour markers are useful in testicular cancer
Serum tumour markers useful for diagnosis, staging and prognosis.
Alpha feto-protein:
AFP is expressed by trophoblastic elements within 50-70% of teratomas. It is not raised in pure seminomas.
Pure choriocarcinoma and pure seminoma do not produce AFP
b-HCG:. hCG is produced by 100% of choricarcinomas, 40% of teratomas, and 10% of seminomas. Only the beta subunit is measured because the a subunit is very similar in the pituitary hormones.
LDH: relatively low specificity. LDG-1 is the most frequently elevated isoenzyme in tesciular cancer.
LDH is elevated in 40%–60% of men with testicular GCTs. Very high LDH levels suggest bulky disease, and rising levels indicate recurrence. Useful as an indicator of tumour burden and treatment response.
Surgical management of testicular cancer
A radical orchidectomy; this uses an inguinal incision, which is the best approach when removing the testis and spermatic cord
What is cryptorchidism
Congenital undescended testis
Treatment of renal stones presenting with nephrosis
Treatment is urgent (within 24 hours of admission), to minimise the risk of rapid deterioration, which relates to the favourable environment for bacteria, and the high pressure in the urinary tract.
After resuscitation, the infected system has to be drained, which for an upper ureteric stone will most easily be done with a ureteric stent placement.
Alternatively, percutaneous nephrostomy tube insertion is an acceptable alternative
When is percutanous nephrostomy insertion preferred to ureteric stent
this is the better option for a distal ureteric stone, as getting the guidewire to pass can be difficult if the stone is distorting the vesico-ureteric junction.
T/F the stone is usually removed at the time of presentation with severe renal colic
Stone removal is not usually attempted at the time of acute presentation, since the inflamed ureter is fragile (risk of rupture) and the irrigant used to visualise the system endoscopically further increases the pressure (greater bacterial translocation into the bloodstream).
What is the definitive treatment of renal stones
Definitive stone treatment follows once the patient is fully cleared of infection, using ureteroscopy (which would most suitable in this case), extracorporeal shock wave lithotripsy (ESWL) or percutaneous nephrolithotomy (PCNL)
What is the indication of percutaneous nephrolithotomy
Percutaneous
Nephrolithotomy (PCNL) is used for the treatment of kidney stones, within the renal collecting system and renal pelvis. It is usually recommended in the following situations:
First line management of staghorn calculi renal stones > 3cm.
Failure of ESWL or stone extraction via Flexible Uretero-renoscopy for renal stones < 3cm
Complications of percutaneous nephrolithotomy
Bowel or spleen or liver injury
Excessive haemorrhage requiring transfusion
Pneumothorax
Damage to intercostals vessels and nerves
Sepsis
What is a hydrocele
An accumulation of fluid within the tunical vaginalis (a serous lining around the testis)
A hydrocoele of the cord (rare) is a fluid collection in part of the processus closed off to the peritoneal cavity and tunica vaginalis
Explain the aetiology / risk factors of hydrocoele
CONGENITAL (=communication), due to a patent processus vaginalis, the peritoneum that follows the descent of the testicle into the scrotum, with failure of obilteration. Peritoneal gluid tracts into the vaginalis. (tie off the patent processus vaginalis)
Acquired: Idiopathic (most common) Infection (epidydmo-orchitis or parasitic infection with wucheria bancrofti or filariasis) Tumour Trauma Underlying torsion of testicle
RISK FACTORS/ASSOCIATIONS
Associated with indirect inguinal hernias in children.
Epididymo-orchitis is common cause in UK
Filariasis is cause of large hydrocoeles in countries of high prevalence
Summarise the epidemiology of hydrocoele
Patent processus vaginalis is very common in male infants, obliterating by age 2.
Hydroceles are common in older men
Filariasis is the most common cause in adults WORLDWIDE
Recognise the presenting symptoms of hydrocoele
Scrotal swelling usually asymptomatic
May be ass. with pain or urinary symptoms due to an underlying cause
Recognise the signs of hydrocoele on physical examination
Scrotal swelling (firm or doughy), in which it is possible to get above the swelling
Transilluminates usually
Difficult to feel the associated tescticle as separate
Identify appropriate investigations for hydrocoele and interpret the results
USS: Shows anechoic fluid collection surrounding anterolateral aspect of the testis. Can also be used to examine for underlying tumours
Urine: Dipstick, MSU for infection
Blood markers for testicular tumours (aFP and bHCG)
Painless lump that can be palpated separate to the testicle
Varicocoele or epididymal cyst
Painless lump that cannot be palpated separate to the testicle
Hydroceole or testicular tumour
Scrotal lump that transilluminates
Hydrocoele or cysts
When is nephrostomy used
It’s just a way to drain urine
If the blockage is in the bladder or due to prostate or urethra, a CATHETER would be used
But if the blockage is higher up then you need a nephrostomy (which is a tube going from the kidney to the skin), which can drain the urine
What investigations should be performed in nephrotic syndrome
…
Struvite stones appear as what
Staghorn calculi (they make up 70% of staghorn calculi)
What are struvite stones cause by
Struvite (magnesium ammonium phosphate)
Occur in setting of infection characterised by urease producting bacteria:
-Proteus, klebsiella, psuedomonas and enterobacter.
How would you investigate a varicocele
Management
You need to do an ultrasound to exclude a renal cancer pressing on the left renal vein.
You only need to treat (which is via embolisation) if symptomatic (i.e. painful), otherwise you can just leave it
T/F a hydrcele can present as a hard mass
Yes it can (it can feel very tight)
You just need to make sure it can transilluminate, and you should still send for an USS to check
Causes of epididymitis and orchiditis
STIs, UTIs and posteropative (TURP/scrotal surgery)
Causes of heaematuria
Cancer
Medical (nephritic syndrome)
Infection
Trauma
Ureteric stone (usually nonvisible)
What type of catheter should NOT be used in a haematuria
Suprapubic…. could put it into a bladder tumour.
Complications of renal tract calculi
Pain
Obstruction of kidney and renal damage
Infection (gram -ve bacteria can cause a life threatening sepsis= INFECTIVE PYELONEPHROSIS)
What are risk factors for development of kidney stones
Underlying metabolic problems:
- Hyperparathyroidism
- Gout
- Cyseinuria
Underlying anatomical problems:
-PUJ-o, MSH, horshoe kidney, ureteric stricture)
What is the first investigation, and then the gold standard investigation if you suspect renal stones
CT KUB is first line and gold standard.
Many stones are radio-opaque, but uric acid stones DO NOT show up on x-ray
they shoqw up on non contast CT KUB which is why this method is gold standard
What are the commonest compositiojn of renal tract calculi
CaO then CaP, uric acid, cysteine, struvite
Struvite (MAP) are the commonest stones wordwide, comapred to CaOx in the UK.
Recurrent pyelonephritis despite treatment with Abx?
Abx won’t penetrate a struvite stone, so check they don’t have one!
What are the examination findings for renal calculi
They must have a completely soft abdomen..
The pain is constant and severe, and there is no rebound tenderness.
If there is guarding/rebound it’s probably something surgical
Why might someone with renal calculi have raised creatinine
They may have been vomiting because of pain and dehydrated.
So the creatinine might be up. Note it is NOT because of reduced renal function as long as the other kidney is functioning fine.
The other kidney will compensate!
T/F a normal urine dipstick excludes renal tract calculi
F.
Up to 1/3 have a normal dipstick
What investigation must be done in emergency dept before patient goes for a CT scan if they present with flank pain
They need a pregnancy test…
it could be a ruptured ectopic, and they are having a CT scan anyway even if the cause is not a rupture ectopic and they’re pregnancy, they can’t have CT
Management of ureteric colic acutely
- Analgesia (morphine, +/- antiemetic) - diclofenac if creatinine normal
- Basic investigations (FBC, u+e, Ca, urate, urine dipstick and bHCG
- Radiological investigations
- Plain BOTH KUB and CT KUB
What is the definitive management of renal tract calculi `
- If stone <10mm, pain controlled and no sepsis. 2 week trial of tamsulosin (relaxes ureter)
2 If you think it’s a uric acid stone (it’s uric acid if it’s visible on CT but not x-ray), you can give potassium citrate to try and dissolve it
- If stone doesn’t pass, surgical management.
If stone between:
0.5cm-2cm= give shockwave lithotripsy (ESWL) or lazer ureteroscopy if it doesn’t work or there are contraindications
If stone >2cm: percutaneous nephorlithotomy. Cut into patient’s sign and tract into kidney. Send ultrasound to break stone up and suction stone out
What are contraindications for ESWL
Anticoagulation, or if it causes them too much pain
What is commonly put in after ureteroscopy/PCNL
A stent, to prevent obstruction of the ureter when the stones are passing
What is obstructive pyonephrosis
Obstruction WITH infection.
Risk of fata gram -ve sepsis
What is the management of obstructive pyonephrosis
Immediate resuscitation and IV antibiotics
Culture
Urgen imaging (KUB and US)
Consider urgent nephrostomy
Monitor closely
In a GP, someone comes in with fever and flank pain, and you suspect pyelonephritis and put them on Abx.
2 days later then come back with no improvement, what’s the next management
It’s likely that it was acutally pyonephrosis.
So you need to send them to hospital to have a KUB in case there’s a stone and obstruction
What operation is used to manage obstructive pyonephrosis
Nephrostomy.
You need to drain the kidney of urine and pus, before treating the underlying stone
So you do a percutaneous nephrostomy
What is the blue dot sign indicative of
Torsion of appendix testis
How is the condition associated with blue dot sign treated
Managed conservaticely ONLY if confident of diagnosis
Investigation for TT
MSU only, there’s no time for anything else
What does acute interstitial nephritis cause symptoms
Acute interstitial nephritis (AIN) is a type of nephritis
that is usually caused by an adverse reaction to a drug. Symptoms of AIN include a
fever, rash, nausea and vomiting.
Young person with HTN what must you always consider
SECONDARY CAUSES!
Examples of nephrotoxic drugs that can cause AKI
. Common examples of nephrotoxic drugs
include ACE inhibitors, NSAIDs, gentamicin and amphotericin.
t/f B-blockers should be stopped acutely in AKI
F. Beta-blockers are not
nephrotoxic and do not need to be stopped acutely
KDIGO criteria for AKI doagnosis
Rise in urea >26mMol in 28hrs
Rise in creatinine >1.5 baseline
Urine output <0.5mL/kg/h for >6hrs
Indications for dialysis in AKI
• Refractory pulmonary oedema
• Persistent hyperkalaemia
• Severe metabolic acidosis
Uraemic complications (e.g. encephalopathy, pericarditis)
• Drug overdose by the BLAST drugs: Barbiturates, Lithium, Alcohol,
Salicylates and Theophyline
How is a UTI defined
A UTI is defined as the presence of a pure growth of > 105 organisms per mL of
fresh MSU. Therefore, an MSU should be sent for microscopy, culture and
sensitivities (MC&S) to confirm a diagnosis of UTI.
What defined CKD
Chronic kidney disease (CKD) is defined as > 3 months of impaired renal function
based on abnormal structure or function, or a GFR < 60 mL/min/1.73m2
for > 3
months with or without evidence of kidney damage.
Symptoms of CKD
60 mL/min/1.73m2
for > 3
months with or without evidence of kidney damage. Symptoms include anorexia,
nausea and vomiting, pruritus, fatigue, peripheral oedema, muscle cramps and
pulmonary oedema. These tend to occur once GFR < 30.
How would you differentiate bergers (IgA) and post streptococcal glomerulonephritis as causes of nephritic syndrome after a pharyngeal infection
Post-streptococcal glomerulonephritis tends to occur 4-6 weeks after a streptococcal
infection (e.g. streptococcal pharyngitis, cellulitis). Whereas IgA nephropathy tends
to occur 5-7 days after the patient experiences symptoms of pharyngitis.
Hypertension is more common in post-streptococcal glomerulonephritis, whereas
heavy proteinuria and systemic symptoms, such as abdominal pain, skin rashes and
arthritis, are more common in IgA nephropathy.
Define chronic kidney disease (CKD)
Staging for CKD
Kidney damage, or GFR <60mL/min/1.73cm2 for 3 months
Kidney damage defined as pathologic abnormalities or markers of damage including abnomralities in blood or urine
GFR. Stage 1. >90 Stage 2. 60-89 Stage 3. 30-59 Stage 4. 15-29 Stage 5. <15
Explain the aetiology / risk factors of chronic kidney disease (CKD)
Most common causes:
1) Diabetes (most common)
- Due to glycation of efferent arteriole increasing pressure in the glomerulus
- So there is at first hyperfiltration, but soon there is glomerulosclerosis and reduced GFR
2) Hypertension
- Arterial walls thicken to withstand increased pressure causing ischaemic injury, glomerulosclerosis and reduced GFR
OTHERS:
Vascular disease: renal artery theroma, vasculitis
Glomerular disease: glomerulonephritis, diabetes, amyloid and SLE
Tubulointerstital disease: pyelonephritis/interstitial nephritis, TB
Obstruction and others: myeloma, HIV nephropathy, scleroderma, gout, renal tumour
CONGENITAL: PCOS, alports syndrome, congential hypoplasia
Summarise the epidemiology of chronic kidney disease (CKD)
Higher incidence in Asian immigrants than native British population
Recognise the presenting symptoms of chronic kidney disease (CKD)
Patients typically present with symptoms of fluid overload (e.g., peripheral edema) and uremia.
Anorexia, nausea, malaise, pruritus
Later: diarrhoea, drowsiness, convulsions and coma
Recognise the signs of chronic kidney disease (CKD) on physical examination
SYSTEMIC:
-Kussmauls (metabolic acidosis), signs of anaemia, oedema, pigmentation, scratch marks, HTN
HANDS:
-Leuconychia, brown line at distal end of nail
AV fistula
Renal bone disease, neuropathy signs
Cardiac arrhtyhmias and pericarditis (due to uraemia, note Uremic pericarditis does not show typical ECG changes such as diffuse ST-segment elevation.)
Identify appropriate investigations for chronic kidney disease (CKD) and interpret the results
1st investigations:
Laboratory evaluation shows hyperkalemia, hyperphosphatemia, and hypocalcemia, as well as metabolic acidosis.
eGFR
Bloods: normocytic, normochromic anaemia. Raised creatinine and urea. Reduced calcium, increased phosphate, AlkPhos and PTH.
Urine: haematuria, proteinuria
Renal USS:
PKD; small kidney size; presence of obstruction/hydronephrosis; kidney stones
What happens to coagulation in chronic kidney disease
↔︎ PT, PTT, platelet count, ↑ bleeding time caused by uremic coagulopathy
How does amiloride work, what about carbonic anhydrase
Amiloride blocks sodium channels within
the collecting tubules and has a similar effect to spironolactone.
Carbonic anhydrase inhibitors act on the proximal convoluted
tubule to increase bicarbonate excretion, which, in turn, increases sodium excretion.
Hypercalcaemia with back pain and a raised ESR?
Hypercalcaemia with back pain
and a raised ESR is suggestive of multiple myeloma - a condition characterised by
proliferation of plasma cells resulting in bone lesions and the production of a
monoclonal immunoglobulin (Ig).
4 main features of multiple myelona
It has four main features, which can be
remembered using the mnemonic ‘CRAB’: Calcium (hypercalcaemia), Renal failure,
Anaemia, Bone pain.
Define urinary tract infection
A UTI is defined as the presence of a pure growth of > 105 organisms per mL of
fresh MSU. However, it is worth noting that up to 1 in 3 women with symptoms of UTI
will have a negative MSU.
How does cystitis present vs pyelonephritis
Cystitis usually presents with frequency, dysuria, urgency and suprapubic pain.
Pyelonephritis causes high fevers, rigors, vomiting and loin pain.
Causes of UTI?
E. coli is the most common cause of UTI. Other causative organisms
include P. mirabilis, K. pneumoniae and S. saprophyticus.
What causes infarction in testicular torsion
Testicular torsion is a surgical emergency in which the spermatic cord twists
resulting in venous outflow obstruction which progresses to arterial occlusion and
testicular infarction.
What test is useful on examination of testicular torsion
The cremasteric
reflex is a useful test when examining a patient with testicular torsion. It is elicited by
lightly stroking the inner thigh, which normally causes ipsilateral contraction of the
cremaster muscle that pulls up the testis. The cremasteric reflex is absent in
testicular torsion. Although it is not a particularly specific test, the presence of the
cremasteric reflex makes testicular torsion very unlikely.
Acute tubular necrosis urine finding?
Muddy brown casts are virtually pathognomonic
What is the cause of acute tubular necrosis
Acute Tubular Necrosis (ATN) is a condition commonly related to episodes of significant hypotension leading to renal hypoperfusion , leading to necrosis of proximal convoluted tubule epithelium.
Toxicology can cause it too: These toxins may include free hemoglobin or myoglobin (e.g. post crush injury), antibiotics (e.g. aminoglycosides ), statins (e.g. atorvastatin ), or cytotoxic drugs (e.g. cisplatin ). Intoxication with ethylene glycol or " anti-freeze " can also cause acute tubular necrosis .
IV catheter infection.
gram-negative , oxidase-negative, catalase-positive , lactose fermenting, rod-shaped bacterium
Enterobacter
aerogenes
IV catheter infection.
a
gram-positive
, catalase-positive , coagulase-negative bacteria that grows in clusters.
Staph epididymis
IV catheter infection. gram-positive , rather than gram-negative , catalase-positive , coagulase -positive cocci that grows in clusters
staph aureus
IV catheter infection. gram-negative , catalase-positive , rod-shaped bacteria that is unable to ferment lactose ,
Pseudomonas aeruginosa
What is seen on biopsy for RPGN
Glomerular crescent formation in at least 50% of glomeruli
Pathologically categorise RPGN
1) Anti-GBM (goodpasture’s-3%)
2) Immune complex (SLE- 45%)
3) Pauci-immune disease (Wegener’s- 50% of cases)
What is urinary tract infection
Characterized by presence of >100,000 of colony-forming units per millilitre of urine.
Urinary tract infections (UTI) may affect bladder (cystitis), kidney (pyelonephritis) or prostate (prostatitis).
Most common causative organism for UTI
Usually transurethral ascent of normal colonic organisms
Most common E.Coli
Other causative organisms for UTI
Usually transurethral ascent of normal colonic organisms
Most common E.Coli
Others includes Proteus mirabilis, Klebsiella and Enterococci (more common in hospitals)
History of UTI
-Cystitis
May be clinically silent (asymptomatic bacturia!)
Cystitis: frequency, urgency, dysuria, haematuria, suprapubic pain, smelly urine
History of UTI
-Pyelonephritis
Loin/Flank pain, fever, malaise, rigors
History of UTI
-Prostatitis
Fever, low back/perineal pain, irritative and obstructive problems
(e.g. hesitancy, urgency, intermittency, poor stream, dribbling)
History of UTI in elderly people
Malaise, nocturia, incontinence, confusion
Examination of UTI:
-Cystitis
Fever, abdominal/suprapubic/loin tenderness, bladder distension
Examination of UTI:
-Pyelonephritis
Fever, loin/flank tenderness.
Examination of UTI:
-Prostatitis
Tender, swollen prostate
Investigations for UTI
What imaging if necessary
1) Dipstick test. For blood, protein, leucocytes, nitrites (urinary bacteria reduce nitrates to nitrites)
MCS: >10^5 colonies/mL indicate a significant bacteruriabut in the presence of UTIsymptoms, the threshold is lower, in women (>102/mL) and in men (>105/mL).
Imaging is renal USS, and IV urogram. Considered for:
- Women with frequent UTIs and
- Children and men
This is to exclude predisposing structural/functional abnormalities.
What is sterile pyuria
Pus cells with no organisms
What might sterile pyuria indicate
Partially treated UTI, tuberculosis stones, tumour, interstitial nephritis or renal papillary necrosis
Management of cystitis
Oral co-trimoxazole, trimethoprim, nitrofurantoin or amoxicillin (females) ciprofloxacin (males)
Mangement of pyelonephritis
IV gentamicin, cefuroxime, or ciprofolacin
Mangement of UTI in a cathetrised patient
Obtain a culture and consider changing the catheter.
Do not treat unless the patient is symptomatic as catheters invariably become colonize
Prophylaxis for UTIs
High fluid intake. Regular micturation to keep bladder empty. Cranberrybased products reduce the frequency of recurrence. In some cases, low-dose long-term (6–12 months) antibiotics for women with frequent UTIs.
Complications of UTI
Renal papillary necrosis (in those with underlying renal disease, e.g. diabetes mellitus or stones).
Renal/perinephric abscess (seen on renal ultrasound).
Pyenephrosis (pus in palvicalyceal system)
Gram negative septicaemia
Prognosis of UTI
- Normally
- Pregnant women
Mostly resolve with treatment. Among pregnant women, 20% develop acute pyelonephritis if not treated
3 types of urinary incontinence
Function- Functional
incontinence is when patients are unable to find a toilet before urinating. It occurs
because of factors like immobility or being in unfamiliar surroundings rather than due
to physiological dysfunction.
Stress- small volume of urine leaks from an incompetent sphincter, whenever there is an increase
in intra-abdominal pressure (e.g. laughing and coughing). It is common in pregnant
women and following childbirth. It is also associated with pelvic floor weakness (e.g.
uterine prolapse).
Urge- Urge incontinence is when the feeling of needing to urinate is
rapidly followed by uncontrollable urination. It results from detrusor overactivity (due
to a neurological problem or an intrinsic problem with the detrusor muscle). Triggers
include the cold, arriving at home and the sound of running water.
What is overflow incontinence
Overflow incontinence is the involuntary release of urine from a full bladder. This
occurs in patients with bladder outflow obstruction or detrusor weakness.
Why is paraphimosis a urological emergency
Paraphimosis is a urological emergency that occurs when a tight foreskin is retracted
and then cannot be replaced back over the glans. The tight foreskin prevents venous
return from the tip of the glans, leading to oedema and, sometimes, ischaemia of the
glans.
t/f paraphimosis can be iatrogenic
It can be iatrogenic - when the foreskin is not replaced after catheterization. It
is usually treated by manually applying pressure to the glans.
Furesomide causes what kind of kidney injury
Acute interstitial nephritis
How is BUN used to establish a cause for AKI
The blood urea nitrogen (BUN)-to- creatinine ratio is usually greater than 20:1 in pre-renal
azotemia
, but 10:1 in obstructive or
renal azotemia
.
Presence of luekocyte casts suggests?
Drug induced interstitial nephritis
What is renal cell carcinoma
Malignancy arising from the renal tubular epithelium
Aetiology of renal carcinoma
Sporadic and hereditary forms are associated with mutations in tumour supressor genes (VHL, TSC) or oncogene (MET)
Hereditary syndrome associated with renal carcinoma
VHL disease, hereditary papillary renal carcinoma etc.
Risk factors for renal carcinoma
Smoking, obesity, tuberous sclerosis, acquired cystic disease of the kidney (chronic dialysis)
Is renal cell carcinoma the most common type of kidney cancer?
Yes, 85% of kidney cancer are renal cell, others include transitional cell carcinoma of the renal pelvis
Hx of renal cell carcinoma
Usually asymptomatic (90%), incidental finding in scanning.
Classic triad of haematuria, flank pain and abdominal mass only seen in 10%
Examination of renal cell carcinoma
May be no signs, HTN, plethora or anaemia.
Palpable renal mass.
In MEN: a left sided tumour extending into the left renal vein can obstruct the left tescticular vein causing a left-sided varicocoele.
Imaging for renal cell carcinoma
First do an abdominal/pelvic USS. Can detect if cystic renal lesions are benign. Detection of masses <2cm is poor.
So better investigation is CT abdo/pelvis (contrast-enhanced) which gives a denfinitve diagnosis. Also allows staging
MRI can be used where contrast dye is contraindicated for CT
CT chest is recommended to complete staging on initial diagnosis to rule out metastatic lesions
Most common metastasis for renal cell carcinoma
Lung (hence do a CT chest on initial diagnosis)
What is epididymitis and orchitis
Inflammation of the epididymis and testes
T/F epidymitis and orchitis commonly occur together
T. 60% of epididymitis is associated with orchitis. Most cases of orchtiis is associated with epidiymitis
Cause of epididymitis and orchitis
Most cases are infective.
Bacterial. If <35 years old, most commonly chlamydia or gonococcal. If >35 years old, most commonly coliforms (E. Coli and enterococcus)
Viral. Mumps, cocksackie, EBV.
Fungal: Candida if immunocompromised
Inflammatory disorders: Behcets and post vastectomy
Orchitis that follows parotitis
Mumps
Hx of epididymitis and orchitis
Painful, swollen, tender testes/epididymis (usually unilateral)
Onset less acute than testicular torsion.
Penile discharge especially in bacterial forms and fever.
Sexual Hx/Hx of parotitis
Examination of epididymitis and orchitis
Erythematous and oedematous scortum
Swollen and tender epidiymis or testis
Walking or eliciting cremaster reflex painful
Palpate parotids
Pyrexia
What is Prehn’s sign
Elevation of scortum alleveviates pain in epididymitis and orchitis but not testicular torsion
Investigations of epididymitis and orchitis
Gram stain of urethral secretions (swab) for gonorrhoea)
Urine microscopy and culture
NAAT (nucleic acid amplification test) of urethral secretions (if urethritis also present) OR first-void urine for Chlamydia, N gonorrhoea, and mycoplasma genitalium
Testicular doppler USS: to exclude torsion if you suspect it (note that if you think it’s actually torsion, you shouldn’t let USS delay an urgent surgical referral)
Abdo USS: to exclude bladder outflow obstruction
Following treatment of acute episode: repeat imaging after resolution should be performed to exclude testicular malignancy
Management of epididymitis and orchitis
Medical: Abx if possible:
YOUNG PATIENTS: Quinolones with activity against chlamydia (e.g. ofloxacin/levofloxacin) for 2 weeks, or doxycycline. Analgesia.
OLDER PATIENTS:
Quinolones (e.g. ciprofloxacin) for 2 weeks, or anti-tiberculous regimen if necessary. Analgesia. Follow up to exclude testiscular malignancy.
SURGICAL EXPLORATION if tescticular torsion cannot be excluded. Also may be necessary in tuberculous cases not responding to medical treatment.
Contact tracing if individual sexually active
Complications of epididymitis and orchitis
Pain, abscess, risk of spreading infection and fourniers gangrene.
Minimal risk to fertility if unilateral and tested.
Testicular atrophy in MUMPS ORCHITIS (if bilateral disease, raised risk of strerility)
A 35-year-old male comes to the emergency department complaining of blood in his urine, severe pain in his left testicle , and left flank pain for 2 hours. He says he has also been very nauseated and vomited an hour before he arrived. Examination shows tenderness to palpation in the left flank, and painful swelling of the testicles
This is likely to be nutcracker syndrome.
It occurs when the left renal vein gets compressed in between the superior mesenteric artery and the abdominal aorta.
This leads to a backing up of blood in the left kidney, leading to haematuria.
In addition, the left renal vein drains the gonads, so if it is blocked you get varicoele in the left testis.
What is the common age for testicular torsion
his is a surgical emergency and commonly occurs between the age of 10 and 15 years (rarely occuring over the age of 21).
T/F in testicular torsion, pain is relieved by elevating the testis
F!!!!!!
in testicular torsion, pain is not relieved by elevating the twisted testis (negative Prehn’s sign), but pain is relieved in acute epidiymitis and
2 main types of malignant tescticular tumours?
What tumour markers do they produce
seminomas (60%) and teratomas (40%)
Teratomas produce both alpha-fetoprotein (α-FP) and beta-human chorionic gonadotrophin (β-hCG), but seminomas only produce the latter.
Which lymph nodes do testicular cancers spread to, and which tissues to they metastasise to?
They may spread to the lungs and liver (via the blood stream) and to the para-aortic lymph nodes (not inguinal!)
How do distinguish pleomorphic adenoma from parotid tumour?
carcinoma would be painful, rapidly growing and may cause facial nerve palsy
Investigation for salivary gland stones
The description of pain and swelling at meal times, when salivary flow is high, is classic. Confirmation of the diagnosis is made with plain X-ray or sialography, which allows examination of the architecture of the salivary gland and duct.
What are red cell casts representative of
Red cell casts are due to red cells being deformed in the distal tubule, so if they are present, then red cells must be leaking into the nephron in the glomerulus or the more proximal tubules.
What is the most common cause of nephrotic syndrome in:
Children
Younger people
Older people
Diabetics
he most common cause in children is minimal change GN, in younger adults it is FSGS and the most common cause in older people is membranous nephropathy. The most common cause in those with a history of long standing DM is diabetic nephropathy.
What is rhabdomyolysis
Rhabdomyolysis is basically myocyte lysis. It may present obviously with a patient having been ‘crushed’ in some way, or may be insidious in onset and not very obvious
An upper range of normal creatinine is always normal, even in a tiny frail lady
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produced constantly by muscle and so one must be careful of accepting a ‘normal’ creatinine in a small frail elderly lady for example (it may be too high for her, given the reduced muscle bulk).
What causes renal failrue in rhabdomyolysis and what is the treatment
in rhabdomyolysis, renal failure is caused by the release of myoglobin from damaged muscle
Expect to also see raised CK (at least 5 times normal), potassium, magnesium and phosphate, and low calcium, with elevated urea and creatinine. Mainstay of treatment is with fluid resuscitation.
Risk factors for bladder cancer
Risk factors include smoking, exposure to carcinogens such as the aromatic amines used in rubber and dye industries, age >55, pelvic radiation and Schistosomiasis resulting in SCC (related to chronic inflammation – so other risks also include UTI, stones etc).
Management for UTI
Antibiotic selection should be based on local guidelines or known sensitivities. Uncomplicated UTIs with no known antibiotic resistance can be treated with co-trimoxazole or nitrofurantoin. If there is resistance, a quinolone can be considered such as ciprofloxacin.
A rough looking homeless man presents to A&E with dysuria, haematuria and frequency. Examination reveals a scrotal mass. Chest x-ray is abnormal.
Renal tuberculosis
T/F the classic triad of haematuria, renal pain and abdo mass is only seen in 10% of patients with renal cell carcinoma
T.
These patients are very commonly asymptomatic and diagnosed incidentally like on imaging when localised malignant looking renal masses are seen.
How might polycystic kidney disease present
Patients may have haematuria (which can be gross), palpable kidneys and symptoms of a UTI which is common in those with the condition.
Hypertension and flank pain are also commonly seen.
Hepatosplenomegaly may also be found.
What is the first investigation for polycystic kidney disease? What is diagnostic
A renal ultrasound is the first test to order when the diagnosis is suspected. If the ultrasound is equivocal, a CT scan can be done of the abdomen and pelvis.
What are the most common type of primary renal cancer
80% are renal cell carcinomas
t/f pregnancy is a risk factor for complicate disease with UTI
T
regnancy is a risk factor for complicated disease as the enlarging uterus compresses the ureters and hormonal changes increase the likelihood of obstructive uropathy.
T/F Abx should begin before culture in acute pyelonephritis
T
Treatment should start before culture results are received to prevent the patient from deteriorating, with empirical antibiotics.
Symptoms of genitourinary TB
GU TB common presents with symptoms of dysuria, haematuria and urinary frequency. Some 20-30% of patients may also be asymptomatic, and sometimes extensive renal destruction may have occured by the time it is diagnosed. Genital TB in men may present as a scrotal mass and in women there may be pelvic pain.
Diagnostic test for GU TB
Diagnosis relies on culturing TB from morning urine samples (3 samples are recommended) or biopsy of the lesion.
T/F CXR is likely to be abnormal in someone with GU TB, as well as tuberculin skin test positive on mantoux testing
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CXR in these patients is abnormal in most cases. Up to 90% are TST positive on Mantoux testing.
Causes of renal artery stenosis
Renal artery stenosis is basically narrowing of the renal artery. It occurs typically due to atherosclerosis or fibromuscular dysplasia.
Presentation of RAS
The presentation tends to be with accelerated or difficult to control hypertension.
What can precipitate AKI in someone with RAS
Acute kidney injury can be seen after starting an ACE inhibitor or an angiotensin II receptor antagonist which this patient has been prescribed. The afferent arteriole is stenosed in RAS and angiotensin II is needed to maintain GFR by constricting the efferent arteriole.
What can AKI cause
he result is this patient has acute renal failure and has developed uraemia. The metabolic acidosis is also as a result of renal failure.
Gold standard RAS test?
What is used in practice?
Conventional angiography (the best test available) has the risk of bleeding and emboli as well as contrast related risks already mentioned.
USS is safe and non-invasive but the sensitivity and specificity is low. CT/MR angiography has the risk of contrast nephropathy and nephrogenic systemic fibrosis.
What is polycystic kidney disease
Autosomal dominant inherited disorder characterized by the development of multiple renal cysts that gradually expand and replace normal kidney substance, variably associated with extrarenal (liver and cardiovascular) abnormalities
Causes of polycystic kidney disease
85% PKD1 (chromosome 16)
15% PKD2 (chromosome 4)
Cysts in PKD are believed to derive from which part of the kidney
Pathological process is considered to be a proliferative/hyperplastic abnormality of the tubular epithelium
Hx of PKD
Usually present at 30–40 years. Twenty percent have no family history. May be asymptomatic.
Pain in flanks due to cyst enlargement/bleeding, stone, blood clot migration, infection.
Can be haematuria, which can be gross
Hypertension
Cardiovascular complication of PKD?
Associated with intracranial “berry” aneurysms and may present with subarachnoid haemorrhage: sudden onset headache
Examination of PKD?
Abdominal distension, enlarged cystic kidneys and liver palpable, hypertension (it is a secondary cause)
Chronic renal failure at late stage
Associated aortic aneurysm or aortic valve disease
Associations of PKD
Extrarenal cysts (hepatic)
Intracranial aneurysms and dolichoectasias (elongated and distended arteries),
aortic root dilation and aneurysms,
mitral valve prolapse,
and abdominal wall hernias.
Associations of PKD
Extrarenal cysts (hepatic and less commonly pancreas)
Intracranial aneurysms and dolichoectasias (elongated and distended arteries),
aortic root dilation and aneurysms,
mitral valve prolapse,
and abdominal wall hernias.
divertuculosis
Investigation for PDK?
If a parent has the gene, and there are large echogenic kidneys (without distinct macroscopy cysts)
on USS in a child, then it is diagnostic
USS:
<30 years of age: at least 2 unilateral or bilateral cysts;
30 to 59 years of age: 2 cysts in each kidney;
> 60 years of age: 4 cysts in each kidney
CT if USS is equivocal.
