Urology Flashcards
What is an acute kidney injury?
An acute kidney injury is characterised by a decline in renal function that happens rapidly (over hours to days)
What classification is an acute kidney injury diagnosed on?
based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria
What are the Kidney Disease: Improving Global Outcomes criteria?
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
Name some risk factors for AKI?
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
Name some pre-renal causes of Acute Kidney Injury?
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)
Name some renal causes of acute kidney injury?
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)
Name some post-renal causes of acute kidney injury?
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)
What classifies as stage 1 AKI?
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
What classifies as stage 2 AKI?
Creatinine rise to 2-2.99x baseline within 7 days
Urine output < than 0.5 mL/kg/hour for more than 12 hours
What classifies as stage 3 AKI?
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
Name some symptoms of AKI?
Nausea and vomiting
Fatigue
Confusion
Anorexia
Pruritus
What do we look for in examination of AKI?
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)
What bedside tests do we do for AKI?
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
What blood tests do we do for AKI?
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
What imaging do we for AKI?
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.
What bloods do we do for an acute renal screen?
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
What is the management for AKI?
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
Name some drugs that may need to be reviewed in AKI?
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.
In AKI what signs would prompt referral for consideration of renal replacement e.g dialysis or haemofiltration?
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)
What are the signs and symptoms of uraemia?
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.
What kind of shock due to sepsis leads to renal hypoperfusion and is a common cause of pre-renal acute kidney injury.
distributive
Iodinated contrast agent is nephrotoxic and increases the risk of AKI - what is a risk factor that increases the chance of an AKI?
Age 75 or over increases the risk of AKI with contrast agents
What is haemolytic uraemic syndrome?
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
An increase by what percentage of creatinine would result in an ACE inhibitor being stopped?
A 30% increase in creatinine levels two weeks after initiating an ACE-inhibitor
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.
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).
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.
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.
What are the signs and symptoms of benign prostatic hyperplasia?
Hesitancy
Weak stream
Frequency
Urgency
Nocturia
Sensation of incomplete emptying
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.
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.
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.
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.
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.
What medication can worsen BPH?
In elderly patients with benign prostatic hyperplasia, anticholinergic medications such as cyclizine can cause or worsen urinary retention.
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
What is bladder cancer?
Bladder cancer is a malignant growth within the urinary bladder.
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.
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
What are the risk factors for squamous cell carcinoma bladder cancer?
Schistosomiasis infection
Long-term catheterisation (10+ years)
What are the risk factors for adenocarcinoma bladder cancer?
Presence of other types of bladder cancer
Local bowel cancer
What are the risk factors for small cell bladder cancer?
Association with other types of bladder cancer
What is the cardinal sign for bladder cancer?
painless visible haematuria
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.
What are the systemic features of bladder cancer?
Unintended weight loss
Night sweats
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).
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.
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.
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).
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.
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
What is dehydration?
Dehydration refers to a state of negative fluid balance, typically resulting from inadequate intake or excessive loss of body fluids.
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.
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.
What investigations does one do for dehydration?
Investigation involves assessment of renal function and electrolytes
What does elevated urea and creatinine levels suggest in dehydration?
suggest prerenal acute kidney injury
What does elevation of urea over creatinine suggest in dehydration?
indicative of gastrointestinal losses.
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).
What are the stages of chronic kidney disease?
stage 1 and stage 2 CKD are defined by reduced eGFR with evidence of kidney damage
What stages of CKD are symptomatic?
Patients are typically asymptomatic until stage 4 or stage 5 CKD.
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.
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
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.
What are the most common causes of chronic kidney disease?
Diabetes
HTN
Polycystic kidney disease
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
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
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)
What is the most common cause of death in CKD?
Cardiovascular disease
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
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
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
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.
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.
What is the type of anaemia in CKD?
normocytic and normochromic
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
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
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
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.
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
What are the contraindications of a kidney transplant?
Uncontrolled infections
Uncontrolled cancer
Life expectancy < 5 years
What are the complications regarding kidney transplant itself?
Early, eg. bleeding, thrombosis, infection, urinary leak, lymphocele
Late, eg. RAS, ureteric stenosis, bladder dysfunction
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.
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
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.
Mangement outline for prostate cancer from notes
Management outline for prostate cancer from quesmed
What is this?
Staghorn calculi made from Struvite
