Renal and Urology Flashcards
1
Q
What is AKI and what are the NICE guidelines for what qualifies as AKI?
A
A rapid drop in kidney function
Increased creatinine > 26micromol/L in 48hrs
Increased creatinine > 50% in 7 days
Urine output <0.5 ml/kg/hr over 6hrs (Oliguria)
2
Q
What are the risk factors for AKI?
A
> 65 years
Sepsis
CKD
HF
Diabetes
Liver disease
Cognitive impairment (leading to reduced fluid intake)
Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
Radiocontrast agents (e.g., used during CT scans
3
Q
What are the pre-renal causes of AKI?
A
Pre-renal (most common):
Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood
Dehydration
Shock (e.g., sepsis or acute blood loss)
Heart failure
Urine osmolality high, urine sodium low
4
Q
What are the renal causes of AKI?
A
Renal causes:
Intrinsic disease in the kidney
Acute tubular necrosis (most common)
Glomerulonephritis
Acute interstitial nephritis
Haemolytic uraemic syndrome
Rhabdomyolysis
5
Q
What are the post-renal causes of AKI?
A
Post-renal:
Obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function (Obstructive uropathy)
Kidney stones
Tumours (e.g., retroperitoneal, bladder or prostate)
Strictures of the ureters or urethra
Benign prostatic hyperplasia (benign enlarged prostate)
Neurogenic bladder
6
Q
What is acute tubular necrosis?
A
Necrosis of the epithelial cells of the renal tubules due to:
- Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
- Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)
granular, muddy brown casts on urinalysis
Cells regenerate 1-3 weeks therefore reversible
7
Q
What is Acute Interstitial Nephritis? What are its features and management?
A
Acute inflammation of the interstitium caused by:
Drugs (NSAIDs,penicillin, rifampicin, allopurinol, furosemide)
Infections (E. coli or HIV)
Autoimmune conditions (sarcoidosis or SLE, Sjorgens syndrome)
Features:
Impaired renal function
‘allergic’ type picture (raised urinary WCC and eosinophils),
Rash
Fever
Flank pain
Eosinophilia
Treat underlying cause. Steroids may reduce inflammation and improve recovery
8
Q
What are the investigations for AKI?
A
U&Es
Urinalysis assesses for protein, blood, leucocytes, nitrites and glucose:
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
Ultrasound of the urinary tract assesses for obstruction when a post-renal cause is suspected.
9
Q
What is the management for AKI?
A
Reverse underlying cause:
IV fluids for dehydration and hypovolemia
Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
Dialysis may be required in severe cases
10
Q
What are some complications of AKI?
A
Fluid overload, heart failure and pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia can cause encephalopathy and pericarditis
11
Q
What differs in U&Es between acute tubular necrosis and prerenal uraemia?
A
Prerenal uraemia - kidneys hold on to sodium to preserve volume
12
Q
What are the staging criteria for AKI?
A
Stage 1:
Increase in creatinine to 1.5-1.9 times baseline
Increase in creatinine by ≥26.5 µmol/L,
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2:
Increase in creatinine to 2.0 to 2.9 times baseline
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3
Increase in creatinine to ≥ 3.0 times baseline
Increase in creatinine to ≥353.6 µmol/L
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours
The initiation of kidney replacement therapy
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
13
Q
When should you refer AKI to a nephrologist?
A
Renal transplant
ITU patient with unknown cause of AKI
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
14
Q
What is CKD and what are some causes?
A
Chronic reduction in kidney function sustained over 3 months. It tends to be permanent and progressive
(<60 mL/min/1.73m² for ≥3 months) and/or kidney damage (proteinuria, haematuria).
Diabetes
Hypertension
Medications (e.g., NSAIDs or lithium)
Glomerulonephritis
Chronic Pylenophritis
Polycystic kidney disease
15
Q
What is the presentation of CKD
A
Most are asymptomatic. Can present with:
Fatigue
Pallor (due to anaemia)
Foamy urine (proteinuria)
Nausea
Loss of appetite
Pruritus (itching)
Oedema
Hypertension
Peripheral neuropathy
16
Q
What are investigations for CKD?
A
eGFR below 60 mL/min/1.73 m2 for 3 months
Proteinuria (ACR) above 3 mg/mmol for 3 months
Haematuria (Urine Dipstick)
Renal Ultrasound
BP
HbA1c
Lipid profile
17
Q
What is the classification of CKD?
A
G1, eGFR >90 A1, ACR< 3 mg/mmol
G2, eGFR 60-89 A2, ACR 3-30 mg/mmol
G3a eGFR 45-59 A3, ACR > 30 mg/mmol
G3b eGFR 30-44
G4, eGFR 15-29
G5, eGFR < 15
18
Q
What is accelerated progression CKD
A
A sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73m2
19
Q
What are some complications of CKD?
A
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
End-stage kidney disease
Dialysis-related complications
20
Q
When should you refer for CKD?
A
eGFR < 30 mL/min
Urine ACR > 70 mg/mmol
Accelerated progression
5-year risk of requiring dialysis over 5%
Uncontrolled hypertension despite 4 or more antihypertensives
21
Q
What can you do to treat the underlying cause of CKD?
A
Optimising diabetic control
Optimising hypertension control
Reducing or avoiding nephrotoxic drugs
Treating glomerulonephritis
22
Q
How can you manage BP in CKD?
A
BP target is 130/80 ( <80yrs) and ACR> 70
ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)
Furosemide for fuid overload
EPO for anaemia related to CKD
Renal replacement therapy (RRT): Dialysis or kidney transplant when GFR is below 15 mL/min/1.73m² or when complications (e.g., uraemia, hyperkalaemia) develop.
23
Q
What medication is prescribed to all patients with CKD for CVD risk?
A
Atorvastatin
24
Q
When are ACE inhibitors offered for hypertension in CKD?
A
Diabetes plus a urine ACR above 3 mg/mmol
Hypertension plus a urine ACR above 30 mg/mmol
All patients with a urine ACR above 70 mg/mmol
25
When are SGLT2 Inhibitors offered for hypertension in CKD?
Offered to patients with:
- Diabetes plus a urine ACR above 30 mg/mmol
Considered for patients with:
- Diabetes plus a urine ACR or 3-30 mg/mmol
- Non-diabetics with an ACR of 22.6 mg/mmol or above
26
How is anaemia of CKD treated?
Oral Iron for 3 months
if the target not reached, IV iron
EPO
27
What are the features of renal bone disease?
Chronic kidney disease-mineral and bone disorder (CKD-MBD)
High serum phosphate
Low vitamin D activity
Low serum calcium
28
What is the management of CKD-MBD?
Reduced dietary intake of phosphate is recommended
First-line:
- Phosphate binders (sevelamer)
- Vitamin D: alfacalcidol, calcitriol
- Parathyroidectomy
29
What is Autosomal dominant polycystic kidney disease (ADPKD)
A genetic condition where the healthy kidney tissue is replaced with many fluid-filled cysts.
The most common inherited cause of CKD (PKD1 and PKD2)
30
What are the diagnostic criteria for ADPKD?
Ultrasound diagnostic criteria:
2 cysts, unilateral or bilateral, if aged < 30 years
2 cysts in both kidneys if aged 30-59 years
4 cysts in both kidneys if aged > 60 years
CT/MRI: For more detailed imaging, especially in patients with equivocal ultrasound findings.
Genetic testing: In some cases, to confirm ADPKD in asymptomatic individuals.
31
What are some symptoms of ADPKD?
Hypertension (early sign due to cyst enlargement).
Abdominal pain from cysts pressing on surrounding structures.
Haematuria (from cyst rupture or bleeding).
Chronic kidney disease with progression to end-stage renal failure in adulthood.
32
What is the treatment for ADPKD?
Antihypertensives for hypertension (e.g., ACE inhibitors)
Analgesia for acute pain
Antibiotics for infections (e.g., UTIs or cyst infections)
Drainage of symptomatic can be performed by aspiration or surgery
Dialysis for end-stage renal failure
Renal transplant for end-stage renal failure
Tolvaptan (vasopressin receptor 2 antagonist if:
CKD G2/3 at the start of treatment
Rapidly progressing CKD
33
What external factors can affect the result of eGFR?
Pregnancy
Muscle mass (e.g. amputees, body-builders)
Eating red meat 12 hours before the sample being taken
34
What are the modifiable and non-modifiable risk factors of diabetic nephropathy?
Modifiable
Hypertension
Hyperlipidaemia
Smoking
Poor glycaemic control
Raised dietary protein
Non-modifiable:
Male sex
Duration of diabetes
Genetic predisposition (e.g. ACE gene polymorphisms)
35
What is the management of diabetic nephropathy?
Screened annually using ACR
should be an early morning specimen
ACR > 2.5 = microalbuminuria
Management
Dietary protein restriction
Blood glucose control: Tight control with insulin or oral hypoglycaemics (e.g., Metformin, SGLT2 inhibitors like Empagliflozin, which may also slow progression of kidney disease).
Blood pressure control: Aim for < 130/80 mmHg, ACE inhibitors (e.g., Ramipril, Lisinopril) or ARBs (e.g., Losartan, Irbesartan) are first-line to reduce proteinuria and slow kidney function decline. If urinary ACR of 3 mg/mmol or more
Statins: Atorvastatin for cardiovascular protection.
Diuretics: To manage fluid retention.
Renal replacement therapy: In end-stage renal disease (ESRD), consider dialysis or kidney transplant.
36
What are the stages of diabetic nephropathy?
Stage 1
- Hyperfiltration: increase in GFR,
may be reversible
Stage 2 (silent or latent phase)
- Most patients do not develop microalbuminuria for 10 years
GFR remains elevated
Stage 3 (incipient nephropathy)
- Microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)
Stage 4 (overt nephropathy)
- Persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
- Hypertension
- Histology shows Kimmelstiel-Wilson nodules
Stage 5
- ESRD, GFR typically < 10ml/min
- Renal replacement therapy needed
37
What is Diabetes Inspidius?
Decreased secretion of ADH from the pituitary (cranial DI)
OR
Insensitivity to ADH (nephrogenic DI).
38
What are some causes of cranial DI?
Idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
Wolframs syndrome/ DIDMOAD (association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness)
haemochromatosis
39
What are some causes of nephrogenic DI?
genetic:
more common form affects the vasopressin (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes:
hypercalcaemia
hypokalemia
lithium
lithium desensitizes the kidney's ability to respond to ADH in the collecting ducts
demeclocycline
tubulointerstitial disease: obstruction, sickle-cell, pyelonephritis
40
What are the features of DI? What investigation would you do and what would you see?
polyuria
polydipsia
Investigation
* Urine osmolality: Very low (hypotonic) urine in the face of hypernatremia (>700 mOsm/kg excludes DI)
* Plasma osmolality: Elevated, due to fluid loss.
* Water deprivation test: To differentiate between central and nephrogenic DI.
* Desmopressin (DDAVP) test: Central DI will respond to DDAVP with a significant reduction in urine output.
* MRI: For imaging the pituitary gland to identify structural abnormalities in central DI.
41
What is the management of DI?
* Central DI:
Desmopressin
* Nephrogenic DI:
Low salt/protein diet
Thiazide diuretics (e.g., Hydrochlorothiazide) to reduce urine output.
Indomethacin (NSAID) may be added to enhance the effect of thiazides.
Amiloride may be used for lithium-induced nephrogenic DI to decrease renal resistance to ADH.
* Fluid management: Ensure adequate water intake to prevent dehydration, particularly in hot weather or when ill.
42
What is Rhabdomyolysis?
Skeletal muscle breaking down and releasing:
Myoglobin
Potassium
Phosphate
Creatine kinase
43
What are some causes of Rhabdomyolysis?
Prolonged immobility, particularly frail patients who fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins
44
What are the signs and symptoms of Rhabdomyolysis?
* Muscle pain, weakness, and swelling.
* Dark (tea-coloured) urine due to myoglobinuria.
* Reduced urine output (oliguria)
* Elevated creatine kinase (CK), lactate dehydrogenase (LDH), and serum potassium.
* Fever, nausea, and confusion in severe cases
* Fatigue
45
What are the investigations for Rhabdomyolysis?
CK: < 150 usually, elevated to 1000-100000, higher = increased risk of kidney injury
Urine dipstick (myoglobinuria)
U&E shows AKI and increased K+
ECG can show increased K+
46
What is the management for Rhabdomyolysis?
IV fluids
IV sodium bicarbonate (to increase urinary pH and reduce the toxic effects of myoglobinuria)
IV mannitol (to increase urine output and reduce oedema
Avoid nephrotoxic agents: Stop medications that may worsen renal function, such as NSAIDs and statins.
47
What are the 3 features of nephrotic syndrome?
1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
48
What are the primary causes of nephrotic syndrome?
Minimal change disease
Focal segmental glomerulosclerosis (FSGS)
Membranous nephropathy
49
What are the secondary causes of nephrotic syndrome?
Diabetes mellitus
Systemic lupus erythematosus (SLE),
Amyloidosis
Infections (HIV, hepatitis B and C),
Drugs (NSAIDs, gold therapy)
50
What is the pathophysiology of nephrotic syndrome?
Damage to the glomerular basement membrane and podocytes leads to increased protein permeability.
This proteinuria results in hypoalbuminaemia and subsequent oedema due to reduced plasma oncotic pressure
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis
Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.
51
What are the investigations for nephrotic syndrome?
Urine dipstick: proteinuria and check for microscopic haematuria
MSU to exclude UTI
Quantify proteinuria using an early morning urinary protein: creatinine ratio or albumin: creatinine ratio
FBC and coagulation screen
U&Es
52
What are some complications of nephrotic syndrome?
Risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
- DVT, PE
- Renal vein thrombosis, resulting in a sudden deterioration in renal function
Hyperlipidaemia
increasing risk of ACS, stroke etc
CKD
Infection due to urinary immunoglobulin loss
Hypocalcaemia (vitamin D and binding protein lost in urine)
53
What are the features of minimal change disease?
Nephrotic syndrome
Normotension - hypertension is rare
Highly selective proteinuria
- only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus
Renal biopsy
- normal glomeruli on light microscopy
- electron microscopy shows the fusion of podocytes and effacement of foot processes
54
What is the management of minimal change disease?
Oral corticosteroids: 80% are steroid-responsive
Cyclophosphamide for steroid-resistant cases
55
What are the causes of FSGS?
Idiopathic
Secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
Heroin
Alport's syndrome
Sickle-cell
56
What is the management of FSGS?
Steroids +/- Immunosuppressants
57
What is membranous glomerulonephritis?
Most common type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure (ESRF). It usually presents with nephrotic syndrome or proteinuria.
Renal biopsy demonstrates:
electron microscopy: the basement membrane is thickened with subepithelial electron-dense deposits. This creates a 'spike and dome' appearance
58
What are some causes of membranous glomerulonephritis?
Idiopathic: due to anti-phospholipase A2 antibodies
Infections: hepatitis B, malaria, syphilis
Malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
Drugs: gold, penicillamine, NSAIDs
Autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
59
What is the management for membranous glomerulonephritis?
ACE inhibitor or ARB
Corticosteroid + cyclophosphamide
Severe or progressive disease requires immunosuppression
Anticoagulation for high-risk patients
60
What is the rule of thirds for membranous glomerulonephritis?
1/3: spontaneous remission
1/3: remain proteinuric
1/3: develop ESRF
61
What is Alport's syndrome?
X-linked dominant pattern.
Defect in the gene coding for type IV collagen = abnormal glomerular-basement membrane (GBM).
Alport's syndrome usually presents in childhood.
62
What are the features of Alport's syndrome?
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus: protrusion of the lens surface into the anterior chamber
Retinitis pigmentosa
Renal biopsy: splitting of lamina densa seen on electron microscopy
63
What is the management for Alport's syndrome?
* Angiotensin-converting enzyme (ACE) inhibitors (e.g., Ramipril, Lisinopril) or Angiotensin receptor blockers (ARBs) (e.g., Losartan, Irbesartan) to reduce proteinuria and slow kidney disease progression
* Steroids (e.g., Prednisolone) for significant proteinuria or glomerulonephritis, although efficacy is variable
* Renal replacement therapy (RRT): Considered when ESRD develops (e.g., haemodialysis or kidney transplant). Renal transplantation with a matched kidney is preferred, but patients should be monitored for recurrence of Alport’s syndrome in the transplanted kidney
* Hearing aids or cochlear implants may be required for hearing loss
* Ophthalmic monitoring: Regular eye exams to detect and manage lenticonus and other ocular issues
64
What is Goodpasture's syndrome?
Anti-glomerular basement membrane (GBM) disease
Small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis
65
What are the features of Goodpastures's syndrome?
Pulmonary haemorrhage
Rapidly progressive glomerulonephritis
Rapid onset acute kidney injury
Nephritis → proteinuria + haematuria
66
What is the management of Goodpastures's syndrome?
Plasmapheresis
Steroids
Cyclophosphamide, Azathioprine
67
What is Haemolytic uraemic syndrome?
Generally seen in young children, caused by Shiga toxin-producing Escherichia coli
Triad of:
- AKI
- Microangiopathic haemolytic anaemia
- Thrombocytopenia
68
What are the investigations for Haemolytic uraemic syndrome?
FBC
- Anaemia: microangiopathic hemolytic anaemia (HB < 8 g/dL with a negative Coomb's test)
- Thrombocytopenia
- Fragmented blood film: schistocytes and helmet cells
U&Es
Stool culture:
- Evidence of STEC infection
- PCR for Shiga toxins
69
What is the management of Haemolytic uraemic syndrome?
* Supportive care:
Fluid and electrolyte balance management (avoid excessive fluid in oliguric phases).
Dialysis: For those with severe AKI or fluid overload
* Antibiotics: Generally not recommended, as they may increase the risk of haemolysis in STEC-induced HUS.
* Plasmapheresis: In severe cases, especially with neurological involvement or poor response to supportive care.
* RBC transfusions: For significant anaemia.
70
What are the key differences between IgA nephropathy and Post-strep glomerulonephritis?
IgA nephropathy
1-2 days after URTI
Young Males
Macroscopic haemturia
PSG
1-2 weeks after URTI
Proteinuria
Low complement
71
What can cause rapidly progressive glomerulonephritis?
Goodpasture's syndrome
Wegener's granulomatosis (GPA)
others: SLE, microscopic polyarteritis
72
What are the features of rapidly progressive glomerulonephritis?
Nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
Features specific to the underlying cause:
- Haemoptysis with Goodpasture's
- Vasculitic rash
- Sinusitis with Wegener's)
73
What are the clinical features of pyelonephritis?
Fever, rigors
Loin pain
Nausea/vomiting
Symptoms of cystitis may be present:
Dysuria
Urinary frequency
74
What are the investigations and management of pyelonephritis?
MSU
* Antibiotics:
First-line: Oral Ciprofloxacin or Co-amoxiclav for uncomplicated cases.
For severe cases: IV Ceftriaxone or Piperacillin-tazobactam.
Pregnant women: IV Cefuroxime or Ceftriaxone
* Pain relief: Paracetamol or NSAIDs for discomfort.
* Hydration: Ensure adequate fluid intake to aid in flushing out the infection.
75
What is Renal cell cancer and what are its features?
Known as hypernephroma and accounts for 85% of primary renal neoplasms. It arises from proximal renal tubular epithelium
classical triad:
- Haematuria, loin pain, abdominal mass
Pyrexia of unknown origin
Endocrine effects
- May secrete erythropoietin (polycythaemia)
- Parathyroid hormone-related protein (hypercalcemia)
- Renin
- ACTH
25% have metastases at presentation
Paraneoplastic hepatic dysfunction syndrome
Varicocele
- Majority left-sided
- Caused by the tumour compressing veins
Stauffer syndrome
- Paraneoplastic disorder associated with renal cell cancer
- Presents as cholestasis/hepatosplenomegaly
76
What are the tumour criteria for Renal cell cancer?
T1: <7cm and confined to the kidney
T2: >7cm and confined to the kidney
T3: Tumour invades major veins or perinephric tissue but not adrenal gland or Gerotas fascia
T4: Tumour invades adrenal gland and Gerotas fascia
77
What is the management of renal cell cancer?
Partial or total nephrectomy depending on the tumour size (T1 tumour = partial nephrectomy)
Alpha-interferon and IL-2 reduce tumour size and also treat patients with metastases
Sorafenib, sunitinib can also be used
78
What is the management for SLE renal complications?
Treat hypertension
Initial therapy:
- Glucocorticoids with either mycophenolate or cyclophosphamide
Subsequent therapy
- Mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease
79
What is the management for renal stones?
Analgesia
- PR/IV diclofenac (CVS events beware)
- Paracetamol IV if insufficient
Alpha Blockers for dilation of ureter (Tamsulosin)
Renal stones
- watchful waiting if < 5mm and asymptomatic
- <20 mm shockwave lithotripsy OR ureteroscopy(pregnant)
- > 20 mm percutaneous nephrolithotomy
Uretic stones
- < 10mm shockwave lithotripsy +/- alpha blockers
- 10-20 mm ureteroscopy
Obstructive pyelonephritis
- Nephrostomy tube
80
What are the investigations for renal stones?
Initial investigations
- Urine dipstick and culture
- Serum creatinine and electrolytes: check renal function
- FBC / CRP: look for associated infection
- Calcium/urate: look for underlying causes
Imaging
- NCCT-KUB within 24hrs
- If fever immediate NCCT-KUB
- Ultrasound for pregnant women and children
- Obstructive pyelonephritis (immediate NCCT-KUB)
81
What are the causes of a normal anion gap?
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
82
What are the causes of a raised anion gap?
lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use
83
What is an anion gap?
(sodium + potassium) - (bicarbonate + chloride)
A normal anion gap is 8-14 mmol/L
84
What are some features of BPH?
BPH typically presents with lower urinary tract symptoms (LUTS), which may be categorised into:
Voiding symptoms (obstructive):
- weak or intermittent urinary flow
- straining
- hesitancy
- terminal dribbling
- incomplete emptying
Storage symptoms (irritative)
- urgency
- frequency
- urgency incontinence
- nocturia
Post-micturition
- dribbling
Complications
- UTI
- retention
- obstructive uropathy
85
What are the investigations for BPH?
Dipstick urine
U&Es: particularly if chronic retention is suspected
PSA: should be done if there are any obstructive symptoms, or if the patient is worried about prostate cancer
Urinary frequency-volume chart
should be done for at least 3 days
International Prostate Symptom Score (IPSS)
Score 20-35: severely symptomatic
Score 8-19: moderately symptomatic
Score 0-7: mildly symptomatic
86
What is the management of BPH?
Watchful Waiting
First Line
- a1 antagonists
- tamsulosin, alfuzosin
Second Line
- 5 alpha-reductase inhibitors
- finasteride
Combination therapy
Surgical Intervention (prostate resection)
87
What is TURP syndrome?
TURP syndrome is a rare and life-threatening complication of transurethral resection of the prostate surgery.
presents with CNS, respiratory and systemic symptoms
88
What are the features of prostatitis?
Pain can be referred to the perineum, penis, rectum or back
Obstructive voiding symptoms may be present
Fever and rigors
DRE: tender, boggy prostate gland
89
What is the management of prostatitis?
* Acute bacterial prostatitis:
Oral antibiotics: First-line treatment includes Trimethoprim, Ciprofloxacin, or Levofloxacin (for 4-6 weeks).
In severe cases, IV antibiotics like Ceftriaxone followed by oral therapy.
* Chronic bacterial prostatitis:
Long-term antibiotics (e.g., Ciprofloxacin, Levofloxacin) for up to 12 weeks.
* Non-bacterial prostatitis: Symptomatic treatment with alpha-blockers (e.g., Tamsulosin) and NSAIDs for pain relief.
* Pelvic floor physical therapy: For chronic prostatitis related to pelvic muscle dysfunction.
* Screen for STI
90
What are the features of prostate cancer?
Localised prostate cancer is often asymptomatic.
Possible features
- bladder outlet obstruction: hesitancy, urinary retention
- haematuria, haematospermia
- pain: back, perineal or testicular
- DRE: asymmetrical, hard, nodular enlargement with loss of median sulcus
91
What are the investigations of prostate cancer?
First Line:
- multiparametric MRI
- previously used to be Transrectal ultrasound-guided biopsy (TRUS)
5-point Likert scale
If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered
If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy
92
What are the PSA thresholds for the different ages?
< 40 Use clinical judgement
40–49 > 2.5
50–59 > 3.5
60–69 > 4.5
70–79 > 6.5
> 79 Use clinical judgement
93
What is the management for localised prostate cancer (T1/T2)?
Conservative: active monitoring & watchful waiting
Radical prostatectomy
Radiotherapy: external beam and brachytherapy
94
What is the management for localised advanced prostate cancer (T3/T4)?
hormonal therapy: Goserelin, Bicalutamide, Cyproterone acetate, Abiraterone
Radical prostatectomy
External beam and brachytherapy
95
What are the complications of radical prostatectomy and external beam and brachytherapy?
Radical prostatectomy
- Erectile Dysfunction
External beam and
- brachytherapyProctitis and are also at increased risk of bladder, colon, and rectal cancer
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What are the features of a hydrocele?
SNT swelling of the hemi-scrotum.
Usually anterior to and below the testicle
the swelling is confined to the scrotum
Transilluminates with a pen torch
Testis may be difficult to palpate if the hydrocele is large
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What is the management of a hydrocele?
infantile hydroceles
- repaired if they do not resolve spontaneously by the age of 1-2 years
Adults
- a conservative approach may be taken depending on the severity of the presentation. Further investigation (e.g. ultrasound) is usually warranted however to exclude any underlying cause such as a tumour
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What are the features and investigations for a varicocele?
Bag of worms
Subfertility
Ultrasound
99
What is the management of a varicocele?
Conservative
Occasionally surgery is required if the patient is troubled by pain.
100
What are the 3 types of bladder cancer?
Urothelial (transitional cell) carcinoma (>90% of cases)
Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis)
Adenocarcinoma (2%)
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What are the features of bladder cancer?
85% will present with painless, macroscopic haematuria
102
What is the treatment of bladder cancer?
Superficial lesions = TURBT
Recurrences/ higher grade/ risk = intravesical chemotherapy.
T2 diseases = radical cystectomy and ileal conduit or radical radiotherapy.
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What are the T-staging criteria for bladder cancer?
T0 No evidence of tumour
Ta Non-invasive papillary carcinoma
T1 Tumour invades sub-epithelial connective tissue
T2a Tumor invades superficial muscularis propria (inner half)
T2b Tumor invades deep muscularis propria (outer half)
T3 Tumour extends to perivesical fat
T4 Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina
T4a Invasion of the uterus, prostate or bowel
T4b Invasion of the pelvic sidewall or abdominal wall
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What are the N-staging criteria for bladder cancer?
N0 No nodal disease
N1 Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node)
N2 Multiple regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node metastasis)
N3 Lymph node metastasis to the common iliac lymph nodes
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What are the M-staging criteria for bladder cancer?
M0 No distant metastasis
M1 Distant disease
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What are the features of cystitis?
More than 6 weeks of:
Suprapubic pain, worse with a full bladder and is often relieved by emptying the bladder
Frequency of urination
Urgency of urination
Symptoms may be worse during menstruation
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What are the investigations of cystitis?
Urinalysis for urinary tract infections
Swabs for sexually transmitted infections
Cystoscopy for bladder cancer
Prostate examination for prostatitis, hypertrophy or cancer
108
What is the management of cystitis?
Supportive ( Bladder retraining, pelvic floor, CBT, Diet, Alcohol)
Anticholinergic medications (e.g., solifenacin or oxybutynin)
Mirebegron (beta-3-adrenergic-receptor agonist)
Cimetidine (histamine-2-receptor antagonist)
Hydrodistention
Surgical Intervention
109
What are the features of an epididymal cyst?
Separate from the body of the testicle
Found posterior to the testicle
110
What is Epididymo-orchitis?
Inflammation of the epididymis.
Orchitis is inflammation of the testicle.
Epididymo-orchitis is usually the result of an infection in the epididymis and testicle on one side.
111
What are the features of Epididymo-orchitis?
Testicular pain
Dragging or heavy sensation
Swelling of testicle and epididymis
Tenderness on palpation, particularly over epididymis
Urethral discharge (should make you think of chlamydia or gonorrhoea)
Systemic symptoms such as fever and potentially sepsis
112
What investigations should be done for Epididymo-orchitis?
Urine microscopy, culture and sensitivity (MC&S)
Chlamydia and gonorrhoea NAAT testing on a first-pass urine
Charcoal swab of purulent urethral discharge for gonorrhoea culture and sensitivities
Saliva swab for PCR testing for mumps, if suspected
Serum antibodies for mumps, if suspected (IgM – acute infection, IgG – previous infection or vaccination)
Ultrasound may be used to assess for torsion or tumours
113
What is the management for Epididymo-orchitis?
Acutely very unwell or septic patients are admitted to the hospital for treatment (IV antibiotics).
Patients at risk of sexually transmitted infection should be referred urgently to genitourinary medicine (GUM) for assessment and treatment.
Enteric organism causing:
- Ofloxacin for 14 days
- Levofloxacin for 10 days
- Co-amoxiclav for 10 days (where quinolones are contraindicated)
STI causing:
- Intramuscular ceftriaxone 500mg IM (single dose) + Doxycycline 100mg BD 10-14days
- Ofloxacin
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What are the features of testicular cancer?
Painless lump on the testicle. Occasionally it can present with testicular pain.
Non-tender (or even reduced sensation)
Arising from testicle
Hard
Irregular
Not fluctuant
No transillumination
Gynaecomastia (Leydig cell tumour)
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What are the 2 types of testicular cancer?
Seminomas
Non-seminomas (mostly teratomas)
116
What are the investigations for testicular cancer?
Scrotal ultrasound
Tumour markers for testicular cancer are:
Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas)
Beta-hCG – may be raised in both teratomas and seminomas
Lactate dehydrogenase (LDH) is a very non-specific tumour marker
Staging CT scan to look for spread
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What are the common places for testicular cancer to metastasise to?
Lymphatics
Lungs
Liver
Brain
118
What is the Royal Marsden staging system:
Testicular staging system:
Stage 1 – isolated to the testicle
Stage 2 – spread to the retroperitoneal lymph nodes
Stage 3 – spread to the lymph nodes above the diaphragm
Stage 4 – metastasised to other organs
119
What is the management for testicular cancer?
Surgery to remove the affected testicle (radical orchidectomy) – a prosthesis can be inserted
Chemotherapy
Radiotherapy
Sperm banking to save sperm for future use, as treatment may cause infertility
120
What is the presentation of UTIs?
Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Haematuria
Cloudy or foul-smelling urine
Confusion is commonly the only symptom in older and frail patients
121
What extra symptoms would occur in pyelonephritis as opposed to UTIs?
Fever
Loin/back pain
Nausea/vomiting
Renal angle tenderness on examination
122
What investigations are used for UTIs and what would be present?
Nitrites – suggest gram -ve bacteria in the urine (E.coli)
Leukocytes - suggest infection
RBC. Microscopic haematuria/ macroscopic haematuria
can present with bladder cancer or nephritis.
MSU will determine the infective organism and the antibiotics that will be effective in treatment. Important in:
Pregnant patients
Patients with recurrent UTIs
Atypical symptoms
When symptoms do not improve with antibiotics
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What is the most common cause of UTIs? What are the other causes?
E.coli
gram-negative, anaerobic, rod-shaped
Other causes:
Klebsiella pneumonia (gram-negative anaerobic rod)
Enterococcus
Pseudomonas aeruginosa
Staphylococcus saprophyticus
Candida albicans (fungal)
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What is the management fo UTIs?
Trimethoprim
Nitrofurantoin (avoided in patients with an eGFR <45)
Alternatives:
- Pivmecillinam
- Amoxicillin
- Cefalexin
Duration of Antibiotics
- 3 days of antibiotics for simple lower urinary tract infections in women
- 5-10 days of antibiotics for immunosuppressed women, abnormal anatomy or impaired kidney function
- 7 days of antibiotics for men, pregnant women or catheter-related UTIs
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What is the management of UTIs in pregnancy?
UTI in pregnancy requires 7 days of antibiotics.
All women should have an MSU
- Nitrofurantoin (avoid in the 3rd trimester) neonatal haemolysis
- Amoxicillin (only after sensitivities are known)
- Cefalexin
Trimethoprim needs to be avoided in the 1st trimester as it works as a folate antagonist. Can cause congenital malformations, particularly neural tube defects (e.g., spina bifida). It is not known to be harmful later in pregnancy but is generally avoided unless necessary.
126
What are the features of urethritis?
Dysuria and/or urethral discharge although it is asymptomatic in up to 30% of men.
127
What are the causes of urethritis?
- Gonococcal urethritis (NGU)
Common causes of NSU
- Chlamydia trachomatis
- Ureaplasma urealyticum
- Mycoplasma genitalium
128
What are the investigations of urethritis?
urethral swab: Gram stained, looking for the presence of leukocytes and Gram-negative diplococci
Chlamydia is now increasingly diagnosed using urinary NAAT
129
What is the management of urethritis?
Oral doxycycline (7 days)
Single dose of oral azithromycin
130
What is the classification of incontinence?
Overactive bladder (OAB)/urge incontinence
- Urge to urinate is quickly followed by uncontrollable leakage ranging from a few drops to complete bladder emptying
Stress incontinence:
- leaking small amounts when coughing or laughing
Mixed incontinence: both urge and stress
overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement
Functional incontinence
- comorbid physical conditions impair the patient's ability to get to a bathroom in time
- dementia, sedating medication and injury/illness resulting in decreased ambulation
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What are the investigations for incontinence?
Bladder diaries should be completed for a minimum of 3 days
Vaginal examination to exclude pelvic organ prolapse and the ability to initiate voluntary contraction of the pelvic floor
muscles ('Kegel' exercises)
Urine dipstick and culture
Urodynamic studies
132
What is the management of Overactive Bladder UI?
Bladder retraining (lasts for a minimum of 6 weeks)
Bladder stabilising drugs: antimuscarinics are first-line
- oxybutynin, tolterodine or darifenacin
- mirabegron in frail elderly patients
133
What is the management of stress UI?
Pelvic floor muscle training
Duloxetine
Surgical intervention
134
What is a clinical indication for dialysis for AKI?
Uraemia (encephalopathy or pericarditis) is an indication for dialysis
135
How do you calculate the Urea: creatinine ratio?
Urea / (creatinine/1000)
136
What is the urine osmolality level for acute tubular necrosis?
Acute tubular necrosis - urine osmolality < 350 mOsm/kg
137
What is a supportive sodium finding for acute tubular necrosis?
Urine sodium > 40 mmol/L
138
What is the screening test for APKD?
Ultrasound abdomen
139
What drug can be used in hypercalciuria and renal stones to cause calcium excretion and reduce stone formation?
Thiazide diurectics
140
What should all patients who have CKD be prescribed?
Statins
141
What is the potassium requirement per day when prescribing fluids?
1 mmol/kg/day
142
What does a disproportional rise in urea compared to creatinine suggest about the AKI presentation?
AKI is due to dehydration
143
What is Nephritic syndrome?
* Nephritic syndrome is characterized by glomerular inflammation due to immune-mediated processes, often following infections (e.g., post-streptococcal glomerulonephritis) or systemic diseases (e.g., lupus nephritis, IgA nephropathy).
* It results in haematuria, hypertension, oedema, and renal insufficiency.
144
What are some features of Nephritic syndrome?
* Haematuria (often with red cell casts)
* Hypertension, oedema (especially periorbital or lower limbs)
* Oliguria and azotaemia (elevated serum creatinine and urea)
* Proteinuria, but less than in nephrotic syndrome
145
What are the investigations for Nephritic syndrome?
* Urinalysis: Red blood cell casts, haematuria, mild proteinuria
* Blood tests: Elevated creatinine, urea, and evidence of inflammation (e.g., elevated CRP, ESR)
* Complement levels: Low C3 in conditions like post-streptococcal glomerulonephritis
* Renal biopsy: To confirm the underlying cause (e.g., immune deposits in lupus nephritis)
146
What is the management for Nephritic syndrome?
* Supportive care:
Control hypertension (using ACE inhibitors or ARBs)
Manage oedema with diuretics (e.g., Furosemide)
* Corticosteroids: In autoimmune causes like lupus nephritis or IgA nephropathy
* Plasmapheresis: In severe or rapidly progressing disease (e.g., Goodpasture’s syndrome)
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