Urology Flashcards
1
Q
What is an acute kidney injury?
A
An acute kidney injury is characterised by a decline in renal function that happens rapidly (over hours to days)
2
Q
What classification is an acute kidney injury diagnosed on?
A
based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria
3
Q
What are the Kidney Disease: Improving Global Outcomes criteria?
A
Increase in serum creatinine by ≥26.5 µmol/l within 48 h, or
Increase in serum creatinine ≥ 1.5x the baseline within the last 7 days, or
Urine output < 0.5 ml/kg/h for 6 hours
4
Q
Name some risk factors for AKI?
A
Patients with CKD
Elderly patients
Previous AKI
Malignancy
Medical conditions increasing risk of urinary obstruction (e.g. benign prostatic hyperplasia)
Cognitive impairment and disability (may be reliant on others for fluid intake)
Recent use of medications such as NSAIDs or ACE inhibitors
Recent administration of iodine-containing contrast media
5
Q
Name some pre-renal causes of Acute Kidney Injury?
A
due to decreased renal perfusion
Hypovolaemia (e.g. dehydration, haemorrhage, gastrointestinal losses, burns)
Renovascular disease (e.g. renal artery stenosis)
Medications reducing blood pressure or renal blood flow (e.g. NSAIDs, ACE inhibitors, ARBs, diuretics)
Hypotension due to reduced cardiac output (e.g. heart failure, sepsis)
6
Q
Name some renal causes of acute kidney injury?
A
due to structural damage to the kidneys
The glomeruli (e.g. acute glomerulonephritis, nephrotic syndrome)
The tubules (e.g. acute tubular necrosis due to ischaemia or toxins, rhabdomyolysis - Muddy brown casts in the urine represent collections of dead renal tubule epithelial cells - results in high fractional excretion of sodium)
The interstitium (e.g. acute interstitial nephritis secondary to drugs)
The renal vessels (e.g. renal vein thrombosis, vasculitis)
7
Q
Name some post-renal causes of acute kidney injury?
A
obstructed to urinary flow anywhere along the urinary tract
Luminal (e.g. ureteric stones or a blocked catheter)
Intramural (e.g. urethral or ureteric strictures, ureteric carcinomas)
Due to external compression (e.g. an abdominal or pelvic tumour, benign prostatic hyperplasia)
8
Q
What classifies as stage 1 AKI?
A
Creatinine rise of 26 micromol/L or more within 48 hours
Creatinine rise to 1.5-1.99x baseline within 7 days
Urine output < 0.5 mL/kg/hour for more than 6 hours
9
Q
What classifies as stage 2 AKI?
A
Creatinine rise to 2-2.99x baseline within 7 days
Urine output < than 0.5 mL/kg/hour for more than 12 hours
10
Q
What classifies as stage 3 AKI?
A
Creatinine rise to 3x baseline or higher within 7 days
Creatinine rise to 354 micromol/L or more with either - Acute rise of 26 micromol/L or more within 48 hours or - 50% or more rise within 7 days
Urine output < than 0.3 mL/kg/hour for 24 hours
Anuria for 12 hours
11
Q
Name some symptoms of AKI?
A
Nausea and vomiting
Fatigue
Confusion
Anorexia
Pruritus
12
Q
What do we look for in examination of AKI?
A
Hypertension (a complication of AKI)
Bladder distension due to urinary retention
Hypotension and dehydration (in many pre-renal causes)
Signs of fluid overload (e.g. raised jugular venous pressure, pulmonary and peripheral oedema) as a complication of AKI
Signs related to the underlying cause (e.g., fevers in sepsis, rashes in vasculitis)
Pericardial rub (in uraemic pericarditis)
13
Q
What bedside tests do we do for AKI?
A
Urinalysis - urine dip may show blood and protein in glomerular disease, increased white blood cells may suggest infection or interstitial nephritis
ECG to screen for complications of hyperkalaemia
Blood gas to look for acidosis as a complication of AKI, allows rapid potassium measurement
14
Q
What blood tests do we do for AKI?
A
U&Es to get creatinine for diagnosis (compare to baseline if available) and check for hyperkalaemia
Full blood count may show anaemia in vasculitis or raised white cells in infection
LFTs may be deranged in severe hypotension causing ischaemic hepatitis
Clotting as a baseline in case a renal biopsy is later required (rare)
Bone profile to screen for hypercalcaemia (seen in myeloma which can cause renal AKI)
Creatinine kinase to look for rhabdomyolysis
CRP may be raised in infection or vasculitis
15
Q
What imaging do we for AKI?
A
Bladder scan if urinary retention is suspected
Ultrasound KUB (kidneys, ureters and bladder) if a post-renal cause is suspected, may show hydronephrosis. The next line of imaging would be a CT KUB as this is a more sensitive modality.
16
Q
What bloods do we do for an acute renal screen?
A
ANA
Double-stranded DNA
Anti-nuclear cytoplasmic antibodies
Anti-GBM antibodies
Erythrocyte sedimentation rate
Serum immunoglobulins
Serum electrophoresis
Serum free light chains
Complement levels (C3 and C4)
HIV screening
Hepatitis B and C serology
If the diagnosis is still unclear and a renal cause is suspected, a renal biopsy may be indicated.
The basic screen is: Protein electrophoresis, C3, C4, ANA, dsDNA, ANCA, anti-GBM, immunoglobulins
17
Q
What is the management for AKI?
A
The key to AKI management is identification and treatment of the underlying cause
The most common cause of AKI is dehydration, and so for many patients IV fluid resuscitation will be required
Careful assessment of fluid status is crucial though, as in certain cases where the patient is fluid overloaded diuretic treatment rather than fluids may be required
Fluid balance should be monitored closely with consideration of catheterisation to monitor urine output
A catheter may be the definitive treatment in some cases (e.g. post-renal AKI due to urethral obstruction)
Screen for complications of AKI (e.g. hyperkalaemia, acidosis, pulmonary oedema) and instigate treatment promptly
Involve the renal team early in severe or complicated AKIs, where the cause is unclear or where a renal cause is suspected
18
Q
Name some drugs that may need to be reviewed in AKI?
A
Review regular medications and suspend any nephrotoxic drugs (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs) and review those that may cause complications in cases of renal impairment (e.g. opiates, metformin)
“Stop the DAMN drugs”
Diuretics and digoxin
ACE inhibitor/ ARB
Metformin and methotrexate
NSAIDs
In the case of metformin NICE advises reducing the dose if eGFR is < 45 ml/min/1.73 m2 and to stop metformin if the eGFR is < 30 ml/min/1.73 m2.
19
Q
In AKI what signs would prompt referral for consideration of renal replacement e.g dialysis or haemofiltration?
A
Acidosis (severe metabolic acidosis with pH of <7.20) - Electrolyte imbalance (resistant hyperkalaemia) - Intoxication (AKI secondary to certain drugs or poisons) - Oedema (refractory pulmonary oedema signified by bibasal crackles on auscultation) - Uraemia (uraemic encephalopathy or pericarditis)
20
Q
What are the signs and symptoms of uraemia?
A
Uraemia caused by acute kidney injury results in the accumulation of urea in the bloodstream, leading to nonspecific symptoms such as nausea, vomiting, confusion, seizures and a characteristic “uraemic tinge” visible on the skin.
21
Q
What kind of shock due to sepsis leads to renal hypoperfusion and is a common cause of pre-renal acute kidney injury.
A
distributive
22
Q
Iodinated contrast agent is nephrotoxic and increases the risk of AKI - what is a risk factor that increases the chance of an AKI?
A
Age 75 or over increases the risk of AKI with contrast agents
23
Q
What is haemolytic uraemic syndrome?
A
classical features of haemolytic uraemic syndrome - with features of bloody diarrhoea, fever, vomiting, acute kidney injury and haemolysis. Most cases occur following an E.coli O157:H7 diarrhoea. Treatment is supportive with fluid rehydration, haemofiltration, steroids and plasmapheresis
24
Q
An increase by what percentage of creatinine would result in an ACE inhibitor being stopped?
A
A 30% increase in creatinine levels two weeks after initiating an ACE-inhibitor
25
In nephrotic patients, sudden onset abdominal pain, haematuria, worsening renal function, and oedema may indicate renal vein thrombosis - what is the best investigation?
a renal Doppler ultrasound is crucial for timely diagnosis and management.
26
What is benign prostatic hyperplasia?
BPH refers to the non-cancerous enlargement of the prostate gland, particularly the transition zone, leading to the compression of the urethra and subsequent lower urinary tract symptoms (LUTS).
27
What causes benign prostatic hyperplasia?
The exact cause of BPH remains unclear, but age and hormonal changes, particularly the influence of dihydrotestosterone (DHT), play pivotal roles in its development. Genetic predisposition and lifestyle factors may also contribute.
28
What is the pathophysiology of benign prostatic hyperplasia?
BPH is characterised by the nodular overgrowth of prostatic tissue, predominantly in the transition zone. This growth impinges on the prostatic urethra, causing dynamic and static obstruction, leading to urinary symptoms.
29
What are the signs and symptoms of benign prostatic hyperplasia?
Hesitancy
Weak stream
Frequency
Urgency
Nocturia
Sensation of incomplete emptying
30
What are the investigations for BPH?
International Prostate Symptom Score (IPSS):
Assessing the severity of LUTS.
Score 20–35: severely symptomatic.
Score 8–19: moderately symptomatic.
Score 0–7: mildly symptomatic.
Digital Rectal Examination (DRE):
To assess prostate size, consistency, and the presence of nodules.
Prostate-Specific Antigen (PSA) Test:
To rule out prostate cancer and guide further investigations.
31
When should one consider the 2 week wait referral pathway for BPH?
As per NICE Guidelines:
Refer men using a suspected cancer pathway referral for prostate cancer if their prostate feels malignant on DRE.
Consider a PSA and DRE to assess for prostate cancer in men with:
Any lower urinary tract symptoms, such as nocturia, urinary frequency, hesitancy, urgency or retention, or
Erectile dysfunction, or
Visible haematuria.
Refer men using a suspected cancer pathway referral (for an appointment within 2 weeks) for prostate cancer if their PSA levels are above the age-specific reference range.
32
What is the conservative management for BPH?
Watchful Waiting:
For mild symptoms, particularly in older individuals.
Lifestyle Modifications:
Fluid restriction, avoidance of caffeine and alcohol, and timed voiding.
33
What is the medical therapy for BPH?
Alpha-blockers (for dynamic obstruction) such as tamsulosin and 5-alpha reductase inhibitors (to reduce prostate size) such as finasteride are commonly prescribed.
If there is an IPSS score of 8 or more, an alpha blocker should be offered. This often provides symptom relief but won't affect prostate growth.
Alpha blockers can cause postural hypotension and should be prescribed with caution in the elderly and those at falls risk.
If the man has an enlarged prostate and is considered to be at high risk of progression, offer a 5-alpha reductase inhibitor, which will reduce prostatic enlargement but can take up to 6 months to show considerable effects.
If the man has bothersome moderate-to-severe voiding symptoms and prostatic enlargement, consider offering a combination of an alpha-blocker and a 5-alpha reductase inhibitor.
34
What is the surgical management for BPH?
Minimally Invasive Therapies:
Procedures like transurethral resection of the prostate (TURP) or laser prostatectomy for moderate to severe symptoms.
Surgical Intervention:
For cases resistant to medical or minimally invasive therapies.
35
What medication can worsen BPH?
In elderly patients with benign prostatic hyperplasia, anticholinergic medications such as cyclizine can cause or worsen urinary retention.
36
What advice should be given regarding PSA tests?
Avoid ejaculation for 48 hours
Ejaculation can temporarily elevate PSA levels, so patients are advised to avoid ejaculation for 48 hours before a PSA test to prevent falsely elevated results
37
What is bladder cancer?
Bladder cancer is a malignant growth within the urinary bladder.
38
What is the most common histological subtype of bladder cancer in developed countries?
transitional cell carcinoma, accounting for 90% of all bladder cancers, followed by squamous cell carcinoma and other types.
39
What are the risk factors for transitional cell carcinoma bladder cancer?
Smoking - biggest risk factor
Exposure to aromatic amines (employed in rubber, dyes, and chemical industry)
Use of Cyclophosphamide
40
What are the risk factors for squamous cell carcinoma bladder cancer?
Schistosomiasis infection
Long-term catheterisation (10+ years)
41
What are the risk factors for adenocarcinoma bladder cancer?
Presence of other types of bladder cancer
Local bowel cancer
42
What are the risk factors for small cell bladder cancer?
Association with other types of bladder cancer
43
What is the cardinal sign for bladder cancer?
painless visible haematuria
44
What are local features of bladder cancer?
Painless haematuria
Recurrent UTIs
Hydronephrosis
Bladder cancer can also invade adjacent structures such as the obturator nerve, resulting in neuropathic pain on the medial thigh.
45
What are the systemic features of bladder cancer?
Unintended weight loss
Night sweats
46
What is the initial bedside investigation for bladder cancer?
Initial bedside investigations include a urine dipstick test to identify haematuria. If there's doubt over the presence of true haematuria, a lab sample can be sent (urine MCS) to confirm the presence of red blood cells, as well as casts (if there are dysmorphic red blood cells it suggests bleeding is glomerular in nature and not from lower urinary tract).
47
What imaging investigations does one do for bladder cancer?
CT Urogram: Contrast is injected into a vein, filtered by the kidney, and excreted into the urinary collecting system. A CT scan then visualises the urinary tract to identify filling defects indicating a tumour.
Flexible cystoscopy: Allows for visualisation of any defects in the bladder and the morphology of any suspicious lesions. If a lesion is identified, a biopsy can be taken.
Further staging investigations may include radiographs, CT scans, MRI scans, and bone isotope scans.
Cystoscopy remains the gold standard investigation to evaluate suspected bladder cancer.
48
What is the 2 week wait referral pathway for bladder cancer?
Refer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for bladder cancer:
If they are aged 45 years and over and have:
Unexplained visible haematuria without urinary tract infection, or
Visible haematuria that persists or recurs after successful treatment of urinary tract infection.
If they are aged 60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test.
Consider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.
49
How does one classify bladder cancer?
Bladder cancer can be classified according to stage and grade, utilising the WHO TNM system. The staging system is based on localised tumour invasion (T), presence of lymph nodes (N), and distant disease (M). Both imaging modalities and pathological specimens are used for staging, with a key objective being differentiation between muscle invasive and non-muscle invasive bladder cancer.
The grade of cancerous cells can be histologically graded from 1-3, with 1 being the least aggressive and 3 the most aggressive.
When it comes to classification and staging the most important aspect is whether the tumour is non-invasive or muscle-invasive as this determines treatment:
Non-muscle invasive: Tis (non-invasive, in situ), Ta – non-invasive, T1 – tumour invades inner lining and connective tissues.
Muscle invasive: T2 (tumour invades muscle), T3 (invades perivesical fat and LN), T4 (metastatic spread).
50
What is the management for non muscle invasive bladder cancer?
This includes stages CIS, Ta, and T1 and is managed with:
Surgery: Transurethral resection of the bladder tumour (TURBT) is the gold standard.
Chemotherapy: The bladder can be instilled with chemotherapeutic agents such as Mitomycin C (single dose if low risk, 6 week course if intermediate risk).
Immunotherapy: BCG immunotherapy can be instilled into the bladders of patients with high-risk non-muscle invasive cancers or carcinoma in situ (CIS).
If there is high-risk muscle non-muscle invasive cancer/CIS a radical cystectomy may still be considered.
51
What is the management for muscle invasive bladder cancer?
This includes any stage from T2 and above. The gold standard treatment is a radical cystectomy with urinary diversion, with options including an ileal conduit, neo-bladder, or Mitrofanoff procedure. Non-surgical treatment options include radiotherapy and chemotherapy, which can be used in both curative and palliative capacities.
This patient has a grade T2 bladder cancer. Cystectomy +/- pelvic lymph node dissection is the gold standard treatment in these patients
52
What is dehydration?
Dehydration refers to a state of negative fluid balance, typically resulting from inadequate intake or excessive loss of body fluids.
53
How does dehydration present?
Clinically, it presents with symptoms such as dry mucous membranes, tachycardia, hypotension and reduced skin turgor. It can be categorised into isotonic, hypertonic or hypotonic dehydration based on alterations in serum osmolarity.
54
What causes dehydration?
diarrhoea, vomiting, polyuria and fever. In certain patient groups such as the elderly or those with impaired cognition, inadequate fluid intake may also contribute significantly.
55
What investigations does one do for dehydration?
Investigation involves assessment of renal function and electrolytes
56
What does elevated urea and creatinine levels suggest in dehydration?
suggest prerenal acute kidney injury
57
What does elevation of urea over creatinine suggest in dehydration?
indicative of gastrointestinal losses.
58
Define chronic kidney disease?
CKD is defined by KDIGO as abnormal kidney function or structure for >3 months. This includes a decreased GFR (below 60 ml/min/1.73m2) or markers of kidney damage (albuminuria, electrolyte abnormalities, structural or histological renal abnormalities).
59
What are the stages of chronic kidney disease?
stage 1 and stage 2 CKD are defined by reduced eGFR with evidence of kidney damage
60
What stages of CKD are symptomatic?
Patients are typically asymptomatic until stage 4 or stage 5 CKD.
61
What does end stage kidney disease mean?
End-stage kidney disease (ESKD) refers to patients with an eGFR of <15 ml/min/1.73m2 or those on dialysis.
62
What are the risk factors for chronic kidney disease?
Risk factors for CKD include the follwing:
Diabetes
Hypertension (HTN)
History of AKI
Cardiovascular diease
Structural renal disease
Systemic disease eg. SLE
Gout
Family history (FH) of CKD
Haematuria or proteinuria
63
What are the investigations for chronic kidney disease?
Bloods: FBC, U&Es, LFTs, HbA1c, bone profile, bicarbonate
Urine: dipstick (looking for blood and protein), microscopy, culture and sensitivities (MC&S) (exclude infection), uPCR/uACR
Renal US: renal size (normal is 10–13 cm) and echotexture, hydronephrosis, structural kidney disease
A 'renal screen' and kidney biopsy may be undertaken if the cause of CKD is not clear.
64
What are the most common causes of chronic kidney disease?
Diabetes
HTN
Polycystic kidney disease
65
How can the causes of CKD be classified?
Glomerular causes can be primary (such as immunoglobulin A (IgA) nephropathy) or secondary (such as SLE)
Vascular causes include vasculitis and RAS
Tubulointerstitial causes include amyloidosis and myeloma
Congenital causes include polycystic kidney disease and Alport syndrome
Systemic causes such as diabetes and HTN
Developmental causes such as vesico-ureteric reflux causing chronic pyelonephritis
66
What are the complications of CKD - best remembered by thinking of the kidney's functions
Waste excretion – uraemia and hyperphosphataemia
Regulation of fluid balance – HTN and peripheral/pulmonary oedema
Acid–base balance – metabolic acidosis
Erythropoietin production – anaemia
Activation of vitamin D – hypocalcaemia
67
What is useful mnemonic to remember the complications of CKD?
CRF HEALS
Cardiovascular disease
Renal osteodystrophy
Fluid (oedema)
Hypertension
Electrolyte disturbance (hyperkalaemia, acidosis)
Anaemia
Leg restlessness (uraemia)
Sensory neuropathy (uraemia)
68
What is the most common cause of death in CKD?
Cardiovascular disease
69
How does one preserve kidney function in CKD?
Lifestyle interventions: maintaining a healthy weight, smoking cessation
HTN: aim for blood pressure (BP) < 140/90 mmHg in patients with CKD and ACR < 70/PCR < 100; or <130/80 mmHg in patients with ACR > 70/PCR > 100 or diabetes
Diabetes: individualised targets but generally aim for HbA1c < 53 mmol/mol
Medication review: any new medications that could be nephrotoxic and need dose adjustment
Offer a statin and consider anti-platelets for the prevention of cardiovascular disease
70
How does one manage the complications of CKD?
HTN: aim for BP < 140/90 mmHg in patients with CKD and ACR < 70/PCR < 100; or <130/80 mmHg in patients with ACR > 70/PCR > 100 or diabetes
Proteinuria: usually managed with ACE-is/ARBs
Anaemia: investigate anaemia as for patients without CKD; consider referral for IV iron/EPO if Hb < 100 g/l (Hb target 100–130 g/l)
CKD–mineral bone disorder (CKD–BMD): managed with dietary phosphate restriction, phosphate binders and activated vitamin D with guidance from Nephrology
Fluid: fluid and salt restriction can be used in conjunction with diuretics
Acid–base status: oral sodium bicarbonate may be prescribed by nephrologists, aiming for a serum bicarbonate level of >22 mEq/l
71
Name the NICE guidance for triggers which leads to referrals for nephrology?
5-year risk of needing kidney replacement therapy of >5% per the kidney failure risk equation
uACR > 70 mg/mmol (unless secondary to diabetes)
uACR > 30 mg/mmol with haematuria
A descrease in eGFR of >25% or change in eGFR category within 12 months
A decrease in eGFR of 15 ml/min/1.73m2 or more per year
Uncontrolled HTN on four agents or more
Suspected genetic cause of CKD
Suspected RAS
72
Explain calcium, phosphate, PTH and vitamin D in the context of chronic kidney disease
In CKD, phosphate accumulates, and there is decreased 1,25(OH)D3, with a low/normal calcium which leads to PTH secretion and secondary hyperparathyroidism.
Secondary hyperparathyroidism leads to abnormal bone turnover (renal osteodystrophy).
Management of CKD-MBD is aimed at keeping calcium and phosphate within normal ranges which includes dietary restriction of phosphate, phosphate binders (eg. sevelamer), activated vitamin D analogues (eg. alfacalcidol), calcimimetics (eg. cinacalcet) and dialysis.
Complications include adynamic bone disease (usually from overtreatment of PTH) and tertiary hyperparathyroidism.
Tertiary hyperparathyroidism results from the autonomous secretion of PTH from the parathyroid glands, which is an indication for surgical parathyroidectomy.
73
What is meant by vascular calcification and how is it linked to CKD?
Vascular calcification refers to the formation of atherosclerotic plaques which leads to myocardial infarction (MI) and stroke, as well as the increased vascular stiffness leading to HTN.
It is thought to be linked to the dysregulation of mineral and bone metabolism in CKD.
It is associated with increased cardiovascular risk and mortality.
74
What is the type of anaemia in CKD?
normocytic and normochromic
75
What cause anaemia in CKD?
Reduced erythropoietin (EPO) production
B12/folate deficiency, malnutrition
Impaired bone-marrow function
Related to dialysis, eg. blood loss, haemolysis
Related to underlying disorder, eg. myeloma, sickle cell disease
Occult malignancy
76
What is the management for anaemia and what are the targets in CKD?
Iron replacement: this can be given orally or IV
EPO administration: erythropoiesis-stimulating agents (ESAs) can be given subcutaneously or IV once iron stores are replete
Targets:
Ferritin >200 µg/l in haemodialysis, >100 µg/l in CKD
Transferrin saturation (TSat) > 20%
Hb 110–120 g/l
77
Complications of haemodialysis?
Cramps, nausea and vomiting
Cardiovascular disease (this is the largest cause of death in dialysis patients)
Dialyser reactions, accidental disconnection, air embolus, hypotension
Fistula-related complications: bleeding, stenosis, thrombosis, aneurysm, infection, steal syndrome, high-output heart failure
Line-related complications: infection, malfunction
Amyloidosis (secondary to build up of B2 microglobulin; rare now, due to change in dialysis membrane)
Dialysis disequilibrium syndrome (acute cerebral oedema due to rapid extraction of osmotically active substances, more common with severe uraemia)
Vascular calcification
Malnutrition
Psychosocial implications
78
Complications of peritoneal dialysis?
One of the major complications of PD is PD peritonitis:
This is typically caused by Gram-positive bacteria, eg. staphylococcus
The patient presents with abdominal pain, fever and a cloudy dialysis bag
The PD fluid should be sent for culture
Management is with intraperitoneal ± systemic antibiotics
Other complications of PD include exit-site and tunnel infections, peritoneal leaks, catheter malfunction and hernias. A rare complication of long-term chronic PD is sclerosing encapsulating peritonitis, where the peritoneal cavity and membrane becomes thickened and calcified, leading to bowel obstruction.
79
Name some initial investigations prior to a kidney transplant
ABO (blood type) and human leukocyte antigen (HLA) type
Virology status: cytomegalovirus (CMV), hepatitis C virus (HCV), hepatitis B virus (HBV), human immunodeficiency virus (HIV), varicella zoster virus (VZV), Epstein–Barr virus (EBV), syphillis, toxoplasma
Assessment of thrombosis risk
Assessment of surgical and anaesthetic risks
Assessment of cardiovascular risk: CXR, ECG, echo (± further CVD assessment/lung-function testing)
Assessment of iliac vessels ± formal angiography
Ultrasound (USS) of native kidneys ± further urological assessment
Screening for malignancy per national guidelines
80
What are the contraindications of a kidney transplant?
Uncontrolled infections
Uncontrolled cancer
Life expectancy < 5 years
81
What are the complications regarding kidney transplant itself?
Early, eg. bleeding, thrombosis, infection, urinary leak, lymphocele
Late, eg. RAS, ureteric stenosis, bladder dysfunction
82
Name the complications caused by a rejection of the transplant?
Hyperacute rejection (within minutes): caused by ABO/HLA incompatibility, presents with graft thrombosis/systemic inflammatory response syndrome (SIRS) within minutes of the transplant and intra-operatively. This is managed by immediate graft removal. This can be prevented by pre-treatment ABO and HLA cross-matching.
Acute rejection (within first 6 months): may be T-cell mediated and/or antibody mediated. Presents with an acute decline in graft. function, and there may also be fever, malaise and graft tenderness
Chronic rejection (>6 months): usually characterised by interstitial fibrosis and tubular atrophy; the underlying mechanisms are not completely understood.
83
Name the side effects of immunosuppressant drugs:
Steroids: insomnia, weight gain, diabetes, HTN, osteoporosis, Cushing syndrome, avascular necrosis of the hip
Calcineurin inhibitors, eg. tacrolimus (TAC), ciclosporin (CIC): nephrotoxicity, HTN, tremor, post-transplant diabetes, hyperkalaemia, hirsutism (CIC) and gumhypertrophy (CIC)
Mycophenolate mofetil (MMF): gastrointestinal (GI) upset, myelosuppression
Azathioprine: myelosuppression
84
Explain the increase risk of infections in kidney transplant patients
Transplant recipients are prone to infection including those present in the general population and more specific immunosuppression related infections
Viral infections eg. HSV, VZV, EBV
CMV: presents with a fever and deranged LFTs, it can affect a number of organ systems
BK virus
Opportunistic infections, eg. aspergillus, pneumocystis pneumonia (PCP)
85
Explain the increase in malignancy in kidney transplant patients?
Transplant recipients are at increased risk of malignancy (2.5–3.0x the general population)
Non-melanoma skin cancer, renal cell and urothelial cell cancers are most common
Post-transplant lymphoproliferative disorder (PTLD) can also occur; EBV is a risk factor
Patients should undergo skin surveillance as well as the national screening for cervical, breast and colorectal malignancies
86
Which blood result would suggest acute kidney disease rather than chronic kidney disease
hyperkalaemia
87
What would you see on an ultrasound of chronic kidney disease?
Chronic kidney disease can progress to end-stage renal disease resulting in shrunken kidneys on ultrasound.
88
Is a low GFR evidence of chronic kidney disease alone?
A low eGFR value is only diagnostic of chronic kidney disease when accompanied by additional supportive evidence such as biopsy-proven glomerulonephritis, persistent haematuria, microalbuminuria or proteinuria or evidence of hereditary kidney disease.
89
What is the recommended threshold for Patients with diabetes and an albumin:creatinine ratio that then require ACE inhibitor treatment to reduce the risk of kidney disease progression.
the value is >2.5mg/mmol in men or >3.5mg/mmol in women
90
Reduced urine output and raised serum creatinine are used in the assessment of what?
Acute kidney injury not chronic!!
91
What variables are used to calculate the Cockcroft-Gault formula measuring creatinine clearance?
age, gender, creatinine and weight
92
A decrease in renal function with associated symptoms of proteinuria and oedema suggest what cause of CKD?
Membranous nephropathy is characterised by the deposition of immune complexes in the glomerular basement membrane leading to proteinuria and nephrotic syndrome. The patient's history of proteinuria and oedema along with a gradual decline in renal function, make membranous nephropathy the most likely cause of her chronic kidney disease.
93
A 60-year-old male with a background of poorly controlled hypertension and smoking presents with a gradual decline in renal function, anaemia and fatigue. He has been experiencing shortness of breath for the past few months.
Which condition is the most likely cause of his chronic kidney disease?
Hypertensive nephrosclerosis is a common cause of chronic kidney disease (CKD) in patients with a history of long-standing hypertension. The patient's history of smoking, a risk factor for hypertension, along with the gradual decline in renal function, anaemia and fatigue, make hypertensive nephrosclerosis the most likely cause of his CKD.
94
Young adults with chronic kidney disease and hypertension can benefit from which drugs due to their protective effect on the kidneys by reducing glomerular hydrostatic pressure without significantly affecting renal blood flow.
ACE Inhibitors
95
What are the guidelines regarding ACE inhibitors in CKD and hypertension?
In managing chronic kidney disease and hypertension with an ACE inhibitor, closely monitor eGFR, creatinine, and potassium levels. If potassium rises above 6.0mmol/L or eGFR decreases from the pre-treatment baseline by <25% OR the serum creatinine increases but not by more than 30%, consider dose adjustment or alternative medication.
96
What is epididymo-orchitis?
a clinical condition characterised by inflammation of the epididymis and the testicle
97
Who gets epididymo-orchitis?
typically occurs in sexually active males, especially those aged 19-35 years. The condition is often associated with sexually transmitted infections in this demographic. However, it can also occur in older males, typically as a complication of urinary tract infections
98
What is epididymo-orchitis commonly caused by?
Sexually transmitted infections, notably chlamydia (commonest cause in those <35) and gonorrhoea
Urinary tract infections, with E. coli being the predominant causative organism in older adults (>35)
99
What are some less common causes of epididymo-orchitis?
Mumps
Tuberculosis
100
What are the signs and symptoms of epididymo-orchitis?
The primary symptom of epididymo-orchitis is acute scrotal pain. Additional signs and symptoms can include:
Testicular swelling and tenderness
Fever
Dysuria (painful urination)
Urethral discharge
Prehn’s positive (lifting up testicle relieves pain due to inflammation)
Cremasteric reflex is intact (this helps differentiate clinically from torsion)
101
What are the investigations for epididymo-orchitis?
Clinical history and physical examination
Urinalysis and urine culture to identify urinary tract infections
Sexually transmitted infection screening via nucleic acid amplification tests (NAATs)
Urethral swab and gram stain can also be performed. If this reveals an intracellular organism Chlamydia is the likely cause, and if it shows grame negative diplococci this suggests Gonorrhoea.
Scrotal ultrasound may be needed to rule out testicular torsion
102
What is the conservative management for epididymo-orchitis?
Symptomatic management with analgesics for pain relief
Scrotal elevation and rest
103
What medication do we give for epididymo-orchitis?
Antibiotics, based on the likely causative organism
High risk for STI: treat empirically with oral doxycycline for 10–14 days, and a single dose of IM ceftriaxone if gonorrhoea is suspected. Referral to sexual health clinic and contact tracing are likely necessary.
If an enteric organism (e.g. E.coli), or UTI is the most likely cause: treat with levofloxacin (10 days) or ofloxacin (14 days). If either of these are contraindicated/not tolerated, co-amoxiclav can be used.
Review after 2 weeks - if ongoing symptoms consider ultrasound imaging +/- urology referral
104
What is nephrotic syndrome?
Nephrotic syndrome is a clinical syndrome that arises secondary to increased permeability of serum proteins through a damaged basement membrane in the renal glomerulus
105
What is the most common cause of nephrotic syndrome in adults?
the most common cause is membranous glomerulonephritis
106
What is the most common cause of nephrotic syndrome in kids?
the primary cause is minimal change disease
107
How to distinguish between nephrotic syndrome and AKI?
To summarize, severe proteinuria, hypoalbuminemia, hyperlipidemia, and generalized edema point toward nephrotic syndrome. Meanwhile, rapid increases in creatinine/BUN and moderate proteinuria suggest AKD, often with an identifiable acute trigger.
108
What systemic diseases cause nephrotic syndrome?
Diabetes Mellitus (Glomerulosclerosis)
Systemic Lupus Erythematosus (Membranous)
Amyloidosis
109
Explain the key features of minimal change glomerulonephritis?
Associated with upper respiratory tract infection
Treat with steroids - if these fail move onto ciclosporin
1% go on to have end-stage renal failure
110
Explain the key features of membranous nephropathy
Associated with cancers (Lung, Colon, Breast), autoimmune conditions (SLE, thyroid disease), infections (Hepatitis B), and drugs (Penicillamine and Gold)
40% have spontaneous remission
Membranous nephropathy results from gradual subepithelial deposits which result in podocyte damage which can be seen as a GBM thickening and a spiked appearance. Treatment consists of ACE inhibitor or ARB and corticosteroid + cyclophosphamide for advanced disease. Prognosis can be remembered by the rule of thirds: one-third of patients will spontaneously recover, one third will have persistent proteinuria and one-third will develop end-stage renal failure.
can be tested for with an anti-phospholipase A2 receptor (PLA2R) antibodies test
Membranous gloreulopathy can cause renal vein thrombosis, this will present with the usual symptoms of nephrotic syndrome (oedema, hypoalbuminaemia and proteinuria) and severe flank pain.
111
Explain the key features of Focal Segmental Glomerulosclerosis
More common in Afro-Caribbean population
Associated with Berger's disease, sickle cell, HIV
Treat with steroids or cylophosphamide/ciclosporin
30-50% progress to end stage renal failure
112
Explain the key features of Membranoproliferative/Mesangiocapillary Glomerulonephritis
Less common
May present as both nephrotic or nephritic
Associated with Hepatitis B, Hepatitis C, and Endocarditis
50% progress to End-Stage Renal Failure
113
Symptoms of nephrotic syndrome?
Proteinuria (>3-3.5g/day)
Oedema (particularly periorbital and peripheral)
Hypoalbuminaemia
Hyperlipidaemia
Lipiduria
114
What are the investigations for nephrotic syndrome?
Urine dipstick: Reveals proteinuria
Urine analysis: Reveals a raised albumin creatinine ratio
Renal biopsy: Indicated in all adults and in children with atypical presentation (e.g., steroid unresponsive, haematuria, under 1 year old or over 12 years old)
115
What is the management for nephrotic syndrome?
Management of Nephrotic Syndrome primarily involves high-dose corticosteroids.
These should be tapered according to clinical response
116
What are the complications of nephrotic syndrome?
Infection: Due to urinary loss of immunoglobulins
Venous thromboembolism: Due to urinary loss of antithrombin III
Hyperlipidaemia: Due to increased hepatic production of lipids to restore the serum oncotic pressures
In nephrotic syndrome, disruption of podocytes leads to proteinuria and reduced intravascular oncotic pressure, which can cause non-dependent oedema and predispose to the development of pleural effusions. A prompt assessment of respiratory status through a chest X-ray is crucial in managing acute dyspnoea.
117
Key differences between nephritic and nephrotic disease?
Nephritic syndrome is characterized by inflammation in the glomeruli, leading to hematuria, mild proteinuria, and often hypertension.
Nephrotic syndrome involves non-inflammatory damage to the glomerular barrier, resulting in massive proteinuria, severe edema, hypoalbuminemia, and hyperlipidemia.
118
A history of haematuria preceded by a recent upper respiratory tract infection suggests what as the most likely cause of proteinuria
IgA nephropathy
This patient is presenting with a classical history of IgA nephropathy, otherwise known as Berger’s disease. This includes episodic haematuria that was preceded by an upper respiratory tract illness. Crucially, this infective episode was only 48 hours prior to developing haematuria, when compared to post-streptococcal glomerulonephritis, when the acute illness precedes haematuria by several weeks
119
Nephrotic syndrome caused by certain medications can lead to hypercoagulability and predispose patients to deep vein thrombosis due to the loss of endogenous anticoagulants.
What medication am I talking about?
caused by regular Penicillamine use. Penicillamine is a copper-chelating agent in Wilson's disease, which can result in membranous nephropathy
120
Define prostate cancer?
Prostate cancer is a malignant tumour that arises from the cells of the prostate, a small walnut-sized gland that produces seminal fluid in men. This condition varies greatly in its presentation, with some cases growing slowly and requiring minimal treatment, while others are aggressive and can spread quickly.
121
What is the main type of prostate cancer and how do they spread?
The majority of prostate cancers are adenocarcinomas, and they usually primarily affect the peripheral prostate. They spread lymphatically first via the obturator nodes.
122
What are non-modifiable risk factors for prostate cancer?
African ethnicity
BRCA gene mutations
Family history of prostate cancer
Age (risk increases with advancing age)
123
What are the modifiable risk factors for prostate cancer?
Obesity
Smoking
Diet rich in animal fats and dairy products
124
Signs and symptoms of prostate cancer?
In its early stages, prostate cancer often produces no symptoms as it affects the peripheral prostate. However, as the disease progresses with local advancement (which can cause compression of the urethra), symptoms may include:
Urinary symptoms, including difficulty initiating or stopping urination
Poor urine stream
Haematospermia (blood in semen)
Pelvic discomfort
Bone pain, potentially indicating metastatic disease
Erectile dysfunction
Bone is the most common site for prostate cancer metastasis, with lower back pain being the most common symptom of advanced disease. Other common symptoms of metastasis include lethargy, anorexia and unintentional weight loss.
Advanced stage prostate cancer commonly metastasize to the spine, which causes metastatic spinal cord compression (limb weakness, difficulty in walking, sensory loss or bladder or bowel dysfunction)
125
What is the initial examination for prostate cancer?
Initial examination should include a digital rectal examination and a urine dip.
First line investigation is a MRI and reported using a 5 point Likert scale
An asymmetrical hard/craggy/nodular prostate with loss median sulcus is suspicious for malignancy.
126
What is the blood test used for prostate cancer?
PSA blood test
127
What are the causes of a falsely elevated PSA?
An active urinary infection or within previous 6 weeks.
Ejaculation in previous 48 hours.
Vigorous exercise, for example cycling, in the previous 48 hours.
Urological intervention such as prostate biopsy in previous 6 weeks.
Acute urinary retention
128
What are the interpretation of PSA results?
After prostatectomy the PSA should fall, although a low and stable level might be present if there is some remaining benign prostate tissue remaining. The PSA can be monitored every 6-12 months for five years post surgery to monitor for recurrence.
129
What is the gold standard radiological investigation for prostate cancer?
Multi-parametric MRI is the gold standard radiological investigation, and can show specific areas which can be targetted for biopsy. If metastatic disease is suspected, additional imaging such as CT scans (can show e.g. sclerotic bony lesions) and bone isotope scans may be required.
Where as ultrasound guided biopsy is the definitive investigation for confirming a diagnosis of prostate cancer.
130
What is the grading system used for the biopsy of prostate cancer?
The Gleason grading system is used to assess prostate cancer severity on initial biopsy. It involves analysing the morphological features of prostatic tissue and assigning a score from 1 (normal tissue) to 5 (very poorly differentiated cells). The sum of the two most common scores represents the Gleason score, which has prognostic value.
-<6=low grade tumour
7=intermediate grade tumour
8-10=high grade tumour
131
What is the 2 week wait referral for prostate cancer?
Refer if their prostate feels malignant on DRE.
Consider referring a person with possible symptoms of prostate cancer using a suspected cancer pathway referral (for an appointment within 2 weeks) if their PSA level is above the threshold for their age (see above)
132
What is the TNM staging for prostate cancer?
T (Tumour):
T1: The tumour is not palpable or visible by imaging.
T1a: Tumour found incidentally in less than 5% of tissue removed.
T1b: Tumour found incidentally in more than 5% of tissue removed.
T1c: Identified by needle biopsy due to elevated PSA (prostate-specific antigen) levels.
T2: The tumour is confined to the prostate.
T2a: Tumour involves half or less of one side of the prostate.
T2b: Tumour involves more than half of one side but not both sides.
T2c: Tumour involves both sides.
T3: The tumour extends beyond the prostate.
T3a: Tumour extends through the prostate capsule.
T3b: Tumor invades seminal vesicle(s).
T4: The tumour invades adjacent structures other than seminal vesicles (e.g., bladder, rectum).
N (Lymph Nodes):
N0: No regional lymph node involvement.
N1: Regional lymph node involvement.
M (Metastasis):
M0: No distant metastasis.
M1: Distant metastasis present.
M1a: Non-regional lymph nodes.
M1b: Bones.
M1c: Other sites or multiple sites.
133
Mangement outline for prostate cancer from notes
134
What is meant by active surveillance for prostate cancer?
This approach is suitable for patients with low-grade prostate cancer and involves repeating investigations periodically to monitor disease progression.
135
What is meant by radiotherapy for prostate cancer?
Radiotherapy can be used either as a curative measure or for palliation to reduce tumour bulk and associated pain.
136
What is meant by surgical management for prostate cancer?
Surgical removal of the prostate and any affected organs is an option for patients without metastatic disease. Minimally invasive techniques such as robotically assisted laparoscopic prostatectomy (RALP) are becoming more common.
Prostatectomy removes the proximal urethral sphincter and changes urethral length. Risk of damage to cavernous nerves ( innervation to bladder and urethra)(7) Damage to cavernous nerves causes ED.
137
What is meant by hormonal management for prostate cancer?
Hormonal therapies aim to reduce testosterone levels, slowing the progression of metastatic prostate cancer. This can be achieved with GnRH analogues, androgen antagonists, or GnRH antagonists. Can cause tumour flares.
Hormonal therapies may cause sexual side effects, including decreased libido, impotence, infertility, and gynecomastia. Metabolic side effects include weight gain, osteoporosis, diabetes, and ischemic heart disease. Haematological side effects include anaemia.
138
Management outline for prostate cancer from quesmed
139
Explain Prostate Imaging-Reporting and Data System (PI-RADS)
PIRADS 1- very low
PIRADS 2- low
PIRADS 3- intermediate/ equivocal
PIRADS 4- high
PIRADS 5- very high
With MMRI Prostate result of PIRADS 3 and above, a biopsy of the prostate (either transperineal biopsy or transrectal ultrasound guided biopsy) should be carried out to diagnose prostate cancer, and grade the tumour by the Gleason scoring system.
140
How does goserilin work in prostate cancer hormone therapy?
Confusingly, goserilin is a gonodotrophin releasing hormone agonist (GnRH agonist). If you remember your endocrine physiology, you will remember that GnRH is secreted intermittently.
What this drug does is increase GnRH secretion leading to continual secretion and subsequently disrupts the hormonal axis.
The end result is reduced secretion of testosterone which reduces growth of the prostate tumour
141
Which of area is the most common site for development of prostate cancer?
More than 75% of prostate adenocarcinomas will originate in the peripheral zone. The clinical significance of this is that development in the peripheral zone causes most prostate cancers to be detectable as palpable nodules or irregular masses on DRE.
Whereas the transitional zone is the most common site for development of benign prostatic hypertrophy (BPH) or benign prostatic enlargement (BPE)
142
Define renal stones and renal colic
Urinary tract stones, or urolithiasis, refer to solid concretions or crystal aggregations formed in the urinary system from substances that are present in urine.
Renal colic is a condition characterised by severe pain caused by the presence of a stone in the urinary tract.
143
What is the most common type of stone?
Calcium oxalate stones: Represent 85% of stones. They are radiopaque e.g picked up on an x-ray, formed in variable urine pH, and majorly linked to hypercalciuria.
144
What is the name of the stone: Account for 10% of stones. They are radiopaque and linked to renal tubular acidosis type 1 & 3, leading to increased urine pH and supersaturation of calcium and phosphate in the urine
Calcium phosphate stones
145
What is the name of the stone:Make up 1% of stones. Characterised by a semi-opaque "ground glass" appearance, they result from inherited recessive inborn errors of metabolism causing disruption in cystine transport and decreased absorption from the renal tubule.
Preventative treatment includes the prescription of penicillamine to reduce the amount of cystine present in the urine.
Cystine stones
146
What is the name of the stone: Comprise 5-10% of stones. They are radiolucent e.g not picked up on an X-ray, formed due to acid produced from purine metabolism and precipitate when urinary pH is low. They can be linked to diseases causing extensive tissue breakdown.
Patients on chemotherapy are at higher risk of urate renal stones, as rapid cell turnover can lead to hyperuricemia and promote the formation of urate stones.
Uric acid stones
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What is the name of the stone: Account for 2-20% of stones. They are radiopaque and formed from magnesium, ammonium, and phosphate, often associated with chronic UTIs from urease producing bacteria like ureaplasma, proteus e.g proteus Mirabilis
Struvite stones
148
What is the name of the stone: Associated with the antiretroviral protease inhibitor Indinavir used in HIV treatment. It can crystallize in renal tubules and result in renal stones. These stones are radiolucent on CTKUB.
Indinavir stones
149
What are the modifiable risk factors for renal stones?
Obesity
Dehydration
Diet rich in oxalate-rich foods like fruits, nuts, and cocoa
150
What are the non-modifiable risk factors for renal stones
Previous stone disease
Anatomical abnormalities of the collecting system
Family history
Underlying medical conditions, such as:
Hyperparathyroidism
Renal tubular acidosis
Myeloproliferative disorders
All chronic diarrhoeal conditions
151
Signs and symptoms of renal stones
Severe, intermittent loin pain that can radiate to the groin ('loin to groin pain')
Restlessness (patients often unable to get comfortable and pace around/ hunch over in pain)
Haematuria – either macroscopic (visible) or microscopic (detected on dipstick only)
Nausea and vomiting
Secondary infection of a stone may cause fever or signs of sepsis, warranting urgent surgical intervention
152
Bedside investigations for renal stones
Urinalysis to detect blood and assist in stone identification for further follow-up. Urinalysis frequently reveals haematuria, although a negative result doesn't exclude renal colic.
Urine MC+S as there may be a co-existing infection/precipitant.
Observations to look for any signs of sepsis which may indicate an infected obstruction, which is a urological emergency.
153
Blood tests for renal stones
Full Blood Count to detect any inflammatory response hinting at an infected system.
Urea and Electrolytes to assess any impairment in renal function.
Calcium & Uric acid to identify underlying metabolic conditions predisposing to stone formation.
154
Radiological investigations for renal stones
A non-contrast helical CT KUB, the gold standard for identifying renal calculi.
An x-ray for managing renal colic if there's a confirmed stone on CT KUB, necessary for the use of extracorporeal shockwave lithotripsy.
155
What do you do if there is evidence of an infected obstruction (i.e. they are septic) with deranged renal function
this is a urological emergency requiring urgent decompression. You don’t remove the stone if someone is infected obstructed, you wait until the infection settles first.
can be achieved with a nephrostomy
Obstructing ureteric calculi, regardless of size, can cause post-renal acute kidney injury, necessitating urgent relief of obstruction through a JJ stent insertion prior to definitive intervention.
156
What analgesics do we give for renal stones?
Commonly IM/PR 75mg/100mg (parenteral routes for better absorption and as patients may be vomiting) diclofenac or strong opiates (codeine).
157
When do we do watchful waiting for renal stones?
Appropriate for stones <5mm with no signs of obstruction, or if the patient prefers non-interventional approaches.
158
When do we do medical expulsive therapy?
Suitable for distal ureter calculi <5mm (e.g., tamsulosin).
159
What do we do for renal stones <2cm
Extracorporeal shockwave lithotripsy (ESWL) (also known as just 'lithotripsy'): High-energy shock waves fragment the stone under fluoroscopic guidance.
Ureteroscopy: Treatment of choice for distal or middle ureteric stones, and for pregnant women. Stents may be placed to prevent ureteric obstruction.
160
What do we do for large (>2cm) stones or complex calculi such as staghorn or cysteine stones.
Percutaneous nephrolithotomy
Open stone surgery: Reserved for complex cases or when other options have failed.
161
What is Hydronephrosis
Hydronephrosis is a condition of the urinary tract where one or both kidneys swell. This happens because pee (urine) doesn’t fully empty from your body. Symptoms may include sudden or intense pain in your back or side, vomiting, painful urination, blood in your pee, or weakness and fever due to a urinary tract infection
162
What is this?
Staghorn calculi made from Struvite
163
What is testicular cancer?
Testicular cancer refers to any malignant neoplasm that originates from the tissues of the testicle.
164
What type are the majority of testicular cancer?
The majority of testicular cancers are germ cell (95%), and these can be seminomas, or non-seminoma subtypes. Non-germ cell testicular cancers include leydig tumours and sarcomas.
Seminoma (55% of cases)
Teratoma (33% of cases)
Mixed seminoma teratoma (12% of cases)
165
Risk factors for testicular cancer?
Age under 45 years
As a general rule, teratomas more commonly occur in younger men, with seminomas in older men
Caucasian ethnicity
Previous history of testicular cancer
Cryptorchidism (undescended testicles)
Human Immunodeficiency Virus (HIV) infection
Previous mumps orchitis infection
Klinefelter's syndrome
166
What are the signs and symptoms of testicular cancer?
The primary clinical manifestation of testicular cancer is a painless lump in the scrotum.
Germ cell tumours may be hormone-producing and can increase the oestrogen:androgen ratio, resulting in gynaecomastia.
167
What are the investigations for testicular cancer?
Scrotal ultrasound: To evaluate the nature and extent of the testicular mass. This is the first-line imaging choice. first line investigation in suspected testicular cancer
Serum tumour markers: These include α-fetoprotein (AFP), human chorionic gonadotropin (hCG), and lactate dehydrogenase (LDH), which aid in the diagnosis and can provide prognostic information.
In non-seminomas of testicular cancer, alpha-fetoprotein (AFP) is the most frequently elevated serum tumour marker where as hCG can be elevated in both seminomatous and non-seminomatous
Further imaging may be necessary if there are concerns about metastatic spread with a CT TAP (noting that testicular cancer first spreads to the para-aortic lymph nodes, and can also spread to the lymph nodes of the chest, and the base of the neck).
firm nodule on the testes with negative transillumination test, think of testicular malignancy
168
What is the management for testicular cancer?
Radical orchidectomy: This surgical procedure involves the removal of the affected testicle, usually the initial step in management.
Radiotherapy: Particularly beneficial for seminomas, which are highly sensitive to radiation.
Chemotherapy: Used as adjuvant therapy or for advanced disease, with cisplatin-based regimens being the most effective.
169
Types of urinary incontinence
Stress incontinence
Urge incontinence
Overflow incontinence
Functional incontinence
Mixed incontinence
170
Name the reversible causes of urinary incontinence:
D - Delirium
I - Infection
A - Atrophic vaginitis or urethritis
P - Pharmaceutical (medications)
P - Psychiatric disorders
E - Endocrine disorders (e.g. diabetes)
R - Restricted mobility
S - Stool impaction
171
Why do we do a physical examination for urinary incontinence?
An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.
172
Why do we do a questionnaires for urinary incontinence?
These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment
173
Why do we do a Bladder diary for urinary incontinence?
These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.
174
Why do we do a urinalysis for urinary incontinence?
This will help to rule out infection as an acute cause
175
Why do we do cystometry for urinary incontinence?
This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.
176
Why do we do a Cystogram for urinary incontinence?
If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.
177
What is stress incontinence?
Complaint of involuntary leakage on effort or exertion, or on sneezing or coughing. This involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.
178
Risk factors for stress incontinence?
Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.
Hysterectomy
179
Triggers for stress incontinence?
Acts such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.
180
Causes for stress incontinence?
Any abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.
181
Conservative management for stress incontinence?
General lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.
Pelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.
182
Medical management for stress incontinence?
Duloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.
183
Surgical management for stress incontinence?
Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.
Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods
Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.
Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.
184
What is urge incontinence?
This involves the sudden and involuntary loss of urine associated with urgency.
185
What are risk factors for urge incontinence?
Recurrent urinary tract infections
High BMI
Advancing age
Smoking
Caffeine
186
What is the conservative management for urge incontinence?
General lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.
First-line management involves a conservative approach with 'bladder training' or 'bladder drill' which aims to re-programme the bladder's muscle to become less overactive.
187
What is the medical/surgical management for urge incontinence?
Pharmacological management
Antimuscarinic (anticholinergic) medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.
Examples include: Oxybutynin, Tolterodine, Fesoterodine, Solifenacin. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).
Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.
Bladder instillation
Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.
Sacral neuromodulation
Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.
188
What is functional incontinence?
This involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.
189
What are the causes of functional incontinence?
Sedating medications
Alcohol
Dementias
In elderly patients with complex medication regimens including opiates and sedatives, functional incontinence may arise due to impaired mobility or cognition.
190
What is overflow incontinence?
This occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.
191
What are the causes of overflow incontinence?
This occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.
192
In urge incontinence what medication would we prefer for elderly?
Mirabegron is a beta-3 adrenergic agonist used to treat urge incontinence. It works by relaxing the detrusor muscle during the storage phase of the bladder fill-void cycle, increasing bladder capacity. This medication is often preferred in elderly patients due to its favorable side effect profile compared to antimuscarinic agents.
193
Name a medication we would avoid in the elderly who have urge incontinence?
Oxybutynin is an antimuscarinic that is effective for urinary urgency but has a higher incidence of anticholinergic side effects, including dry mouth, blurred vision, constipation, and cognitive effects, which can be significant, especially in elderly patients, where there can also be an increased risk of falls. It is generally less preferred compared to mirabegron.
194
What is the diagnosis of constant leaking of urine with factors of difficult and prolonged labour?
Vesicovaginal Fistula
195
What is a lower urinary tract infection?
A lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.
196
What causes lower urinary tract infections?
LUTIs are caused by the transurethral ascent of colonic commensals, most commonly E. coli.
197
What are the signs and symptoms of lower urinary tract infections?
Urinary frequency
Dysuria
Urgency
Foul-smelling urine
Suprapubic pain
Clinical examination may be normal or reveal suprapubic tenderness.
198
What are the red flag symptoms of urinary tract infections?
Red flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.
199
What are the investigations for a lower urinary tract infection?
Urine dipstick is positive for leucocytes and nitrites in most cases.
In uncomplicated cases, no further investigations are required.
In children, men, and pregnant women a mid-stream urine sample should be sent.
NB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.
200
If a lower urinary tract infection is being managed in secondary care due to red flag symptoms what are the investigations?
If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.
For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.
201
What is the management for lower urinary tract infections in most cases?
First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.
The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.
202
What is the management for lower urinary tract infections in men?
Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for 7 days.
Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.
203
What is the management for a lower urinary tract infection in women who are pregnant with no harmaturia?
First-line antibiotics are nitrofurantoin (but avoid at term - in breastfeeding women the BNF advises that it should be avoided due to the risk of it causing haemolysis in glucose-6-phosphate dehydrogenase deficient babies, as small amounts of it will be transmitted via breast milk. ), for 7 days.
If nitrofurantoin is not suitable due to e.g. renal function (an eGFR of less than 45) or G6PD deficiency, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefelexin for 7 days.
Trimethoprim can be used in the 3rd trimester (though should be strictly avoided in 1st trimester due to the increased risk of neural tube defects, since it is a folate antagonist), and may be considered if a woman has UTI but has a penicillin allergy
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What is Pyelonephritis?
a urinary tract infection affecting the kidneys/renal pelvis.
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What are the clinical features of pyelonephritis?
Clinical features
Patients with pyelonephritis generally present with:
Fever/rigors
Malaise
Loin/flank pain
Vomiting
Clinical examination reveals fever and loin/flank tenderness.
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What are the investigations for pyelonephritis?
Bedside tests include a urine dipstick which will typically be positive for leucocytes and nitrites.
After admitting the patient, blood tests should be taken to include Full Blood Count (raised WCC), Urea and Electrolytes (to check for renal impairment), and blood cultures.
Other investigations include a urine MSU for microscopy, culture, and sensitivity.
A renal ultrasound can be performed to look for hydronephrosis if severe infection occurs with acute kidney injury.
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What is the management of pyelonephritis?
The patient should be admitted to hospital for intravenous antibiotics (broad-spectrum cephalosporin, a quinolone, or gentamicin).
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If taking methotrexate and you have a UTI which drug should you avoid?
avoid trimethoprim - increases the risk of bone marrow suppression
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How does trimethoprim affect renal function?
Trimethoprim can cause competitive inhibition of creatinine secretion from renal tubules, leading to falsely low estimated glomerular filtration rates.
