Renal & Urology Flashcards
Learning objectives
Answer
Define acute kidney injury (AKI)
An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
o NOTE: this can occur in patients with previously normal kidneys or in patients with pre-existing renal disease
• KDIGO Classification of AKI
o Increase in serum creatinine > 26 mol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for 6 hours nine >26 umol/l within 48 hours/ to >1.5 times baseline within the preceeding 7 days/ urine volume <0.5 ml/kg/hr for 6 hours
Explain the aetiology / risk factors of acute kidney injury (AKI)
Pre renal (90%) - Hypovolaemia (e.g. haemorrhage, severe vomiting), heart failure, cirrhosis, nephrotic syndrome, hypotension (e.g. shock, sepsis, anaphylaxis), renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis). Intrinsic renal - glomerular - glomerulonephritis, haemolytic yuraemic syndrome, Tubular - acute interstitial necrosis, Interstitial (e.g. NSAIDs, autoimmune), Vasculitides (e.g. Wegener’s granulomatosis), Eclampsia. Post renal (due to obstruction) - Calculi, Urethral Structure, Prostatic hypertrophy or malignancy, Bladder tumour. Risk Factors: Age, CKD, Comorbidities (e.g HF), Sepsis, Hypovolaemia, Use of nephrotoxis medications, Emergency surgery, Diabetic mellitus
Summarise the epidemiology of acute kidney injury (AKI)
15% of adults admitted to hospital. Most common in the elderly.
Recognise the presenting symptoms of acute kidney injury (AKI)
Dependent on the underlying cause. Oligura/anuria (abrupt anuria suggests post-renal obstruction. Nausea/vomiting, dehydration, confusion
Recognise the signs of acute kidney injury (AKI) on physical examination
Hypertension, distended bladder, dehydration - postural hypotension, fluid overload (in HF, cirrhosis, nephrotic syndrome), - raised JVP, pulmonary and peripheral oedema, pallor, rash, bruising (vascular disease)
Identify appropriate investigations for acute kidney injury (AKI) and interpret the results
Urinalysis - blood (suggests nephritic cause), Leucocyte esterase and nitrites - UTI, Glucose, Protein, Urine osmolality. Bloods - FBC, Blood Film, U & Es, Clotting, CRP, Immunology - • Serum immunoglobulins and protein electrophoresis - for multiple myeloma - Also check for Bence-Jones proteins in the urine
• ANA - associated with SLE - Also check anti-dsDNA antibodies (high in active lupus)
• Complement levels - low in active lupus
• Anti-GBM antibodies - Goodpasture’s syndrome
• Antistreptolysin-O antibodies - high after Streptococcal infection . Virology- Hep & HIV, Ultrasound - Post renal cause - look for hydronephrosis, CXR - Pulmonary Oedema, AXR - Renal stones
Generate a management plan for acute kidney injury (AKI)
Treat the cause
FOUR main components to management:
o Protect patient from hyperkalaemia (calcium gluconate)
o Optimise fluid balance
o Stop nephrotoxic drugs
o Consider for dialysis
Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrology if intrinsic renal disease is suspected
Renal Replacement Therapy (RRT) considered if:
o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications
Identify the possible complications of acute kidney injury (AKI) and its management
- Pulmonary oedema
- Acidaemia
- Uraemia
- Hyperkalaemia
- Bleeding
Summarise the prognosis for patients with acute kidney injury (AKI)
Inpatient mortality varies depending on cause and comorbidities Indicators of poor prognosis: o Age o Multiple organ failure o Oliguria o Hypotension o CKD Patients who develop AKI are at increased risk of developing CKD
Define amyloidosis
• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils
Explain the aetiology / risk factors of amyloidosis
• Amyloid fibrils are polymers of low-molecular-weight subunit proteins
• These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
• Their deposition progressively disrupts the structure and function of normal tissue
• Amyloidosis is classified according to the fibril subunit proteins
o Type AA - serum amyloid A protein
o Type AL - monoclonal immunoglobulin light chains
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
Summarise the epidemiology of amyloidosis
- AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
- AL - 300-600 cases in the UK per year
- Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
Recognise the presenting symptoms & signs of amyloidosis
- Renal - proteinuria, nephrotic syndrome, renal failure
- Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
- GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
- Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
- Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
- Joints - painful asymmetrical large joints, enlargement of anterior shoulder
- Haematological - bleeding tendency
Identify appropriate investigations for amyloidosis and interpret the results
• Tissue Biopsy • Urine - check for proteinuria, free immunoglobulin light chains (in AL) • Bloods o CRP/ESR o Rheumatoid factor o Immunoglobulin levels o Serum protein electrophoresis o LFTs o U&Es • SAP Scan - radiolabelled SAP will localise the deposits of amyloid
Define benign prostatic hyperplasia
- Slowly progressive nodular hyperplasia of the periurethral (transitional) zone of the prostate gland
- It is the most frequent cause of LUTS in adult males
Explain the aetiology/risk factors of benign prostatic hyperplasia
- UNKNOWN
- Link with hormonal changes (e.g. androgens)
- Risk Factors: reduced risk with soya/vegetable based diets and negative association with cirrhosis
Summaries the epidemiology of benign prostatic hyperplasia
- COMMON
- 70% of men > 70 yrs have histological BPH (50% of them will experience symptoms)
- More common in the west than the east
- More common in Afro-Caribbeans
Recognise the presenting symptoms of benign prostatic hyperplasia
• Obstructive Symptoms o Hesitancy o Poor or intermittent stream o Terminal dribbling o Incomplete voiding • Irritative/Storage Symptoms o Frequency o Urgency o Urge incontinence (leakage of urine that accompanies an intense desire to pass water with failure of restraint) o Nocturia • TIP: the obstructive and irritative symptoms can be remembered using the mnemonic FUND HIPS o Frequency o Urgency o Nocturia o Dysuria o Hesitancy o Incomplete voiding o Poor stream o Smell/odour • Acute Retention Symptoms o Sudden inability to pass urine o Associated with SEVERE PAIN • Chronic Retention Symptoms o Painless o Frequency - with passage of small volumes of urine o Nocturia is a major feature
Recognise the signs of benign prostatic hyperplasia on physical examination
• DRE - the prostate is usually smoothly enlarged with a palpable midline groove
• NOTE: there is poor correlation between the size and the severity of the symptoms
• Signs of Acute Retention
o Suprapubic pain
o Distended, palpable bladder
• Signs of Chronic Retention
o A large distended painless bladder (volume > 1 L)
o Signs of renal failure
Identify appropriate investigations for benign prostatic hyperplasia
• Urinalysis
o Check for UTI signs and blood
• Bloods
o U&Es - check for impaired renal function
o PSA
• Midstream Urine
o MC&S
• Imaging
o US of urinary tract (check for hydronephrosis)
o Bladder scanning to measure pre- and postvoiding volumes
o Transrectal Ultrasound Scan (TRUS) - allows assessment of bladder size and volume
o Flexible Cystoscopy
Generate a management plan for benign prostatic hyperplasia
• In Emergency (acute urinary retention) o Catheterisation • Conservative (if mild) o Watchful waiting • Medical o Selective a-blockers (e.g. tamsulosin) relax the smooth muscle of the internal urinary sphincter and prostate capsule o 5a-reductase inhibitors (e.g. finasteride) will inhibit the conversion of testosterone to dihydrotestosterone, which can reduce prostate size by around 20% • Surgery o TURP o Open prostatectomy
Identify possible complications of benign prostatic hyperplasia
• Recurrent UTI • Acute or chronic urinary retention • Urinary stasis • Bladder diverticula • Stone development • Obstructive renal failure • Post-obstructive diuresis • Complications of TURP o Retrograde ejaculation (you ejaculate up into your bladder because the internal urinary sphincter is relaxed) o Haemorrhage o Incontinence o TURP syndrome • DEFINITION: seizures or cardiovascular collapse caused by hypervolaemia and hyponatraemia due to absorption of glycine irrigation fluid o Urinary infection o Erectile dysfunction o Urethral stricture
Summarise the prognosis for patients with benign prostatic hyperplasia
- Mild symptoms are usually well controlled medically
* Most patients get significant relief from surgery