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
Define bladder cancer
• Malignancy of bladder cells
o Most bladder cancers are transitional cell carcinomas
o RARELY, bladder cancers may be squamous cell carcinomas associated with chronic inflammation (e.g. schistosomiasis)
Explain the aetiology / risk factors of bladder cancer
• UNKNOWN • Risk Factors o Smoking o Dye stuffs (naphthylamines and benzidine) o Cyclophosphamide treatment o Pelvic irradiation o Chronic UTIs o Schistosomiasis
Summarise the epidemiology of bladder cancer
- 2% of cancers
- 2nd most common cancer of the genitourinary tract
- 2-3 x more common in MALES
- Peak incidence: 50-70 yrs
Recognise the presenting symptoms of bladder cancer
• Painless macroscopic haematuria • Irritative/storage symptoms o Frequency o Urgency o Nocturia • Recurrent UTIs • Rarely: ureteral obstruction
Recognise the signs of bladder cancer on physical examination
- Often NO SIGNS
* Bimanual examination may be performed as part of disease staging
Identify appropriate investigations for bladder cancer and interpret the results
- Cystoscopy - allows visualisation, biopsy or removal
- Ultrasound
- Intravenous urography
- CT/MRI for staging
Define chronic kidney disease (CKD)
• Progressive loss of kidney function over a period of months or years
• The definition is based on the presence of kidney damage or decreased kidney function (i.e. eGFR < 60 ml/min per 1.73 m2) for three months or more
• Classification of CKD
o Stage 1: Normal
• eGFR > 90 ml/min per 1.73 m2 with other evidence of CKD (microalbuminuria, proteinuria, haematuria, structural abnormalities, biopsy showing glomerulonephritis)
o Stage 2: Mild Impairment
• eGFR 60-89 ml/min per 1.73 m2 with other evidence of CKD
o Stage 3a: Moderate Impairment
• eGFR 45-59 ml/min per 1.73 m2
o Stage 3b: Moderate Impairment
• eGFR 30-44 ml/min per 1.73 m2
o Stage 4: Severe Impairment
• eGFR 15-29 ml/min per 1.73 m2
o Stage 5: Established Renal Failure
• eGFR < 15 ml/min per 1.73 m2 or on dialysis
Explain the aetiology/risk factors of CKD
• In developed countries it is mainly associated with: o Age o Diabetes mellitus o Hypertension o Obesity o Cardiovascular disease • Other risk factors: o Arteriopathic renal disease o Nephropathies o Family history o Neoplasia o Myeloma o Systemic disease (e.g. SLE) o Smoking o Chronic use of NSAIDs
Summarise the epidemiology of CKD
- COMMON
- Risk increases with age
- Often associated with other diseases (e.g. cardiovascular disease)
Recognise the presenting symptoms of CKD
• Often ASYMPTOMATIC • May be an incidental finding of a routine blood or urine test • Symptoms of Severe CKD: o Anorexia o Nausea and vomiting o Fatigue o Pruritus o Peripheral oedema o Muscle cramps o Pulmonary oedema • Sexual dysfunction is common
Recognise the signs of CKD on physical examination
• Physical examination rarely reveals many clues
• May show signs of underlying disease (e.g. SLE)
• May show complications of CKD (e.g. anaemia)
• Signs of CKD:
o Skin pigmentation
o Excoriation marks
o Pallor
o Hypertension
o Peripheral oedema
o Peripheral vascular disease
Identify appropriate investigations for CKD
• Assessment of Renal Function
o Urea - not ideal because it varies massively depending on hydration status and diet
o Creatinine - useful but has limitations. Renal function can drop considerably with minimal change in serum creatinine
o Isotopic GFR - GOLD STANDARD but expensive
• Biochemistry
o Glucose - check for undiagnosed diabetes and diabetic control
o Potassium - raised
o Also check sodium, bicarbonate, calcium, phosphate
• Serology
o Antibodies
• ANA - SLE
• c-ANCA - granulomatosis with polyangiitis (Wegener’s)
• Anti-GBM - Goodpasture’s syndrome
o Hepatitis serology
o HIV serology
• Urinalysis
o Check for proteinuria/haematuria
o 24 hr urine collection
o Serum or urine protein electrophoresis - check for multiple myeloma
• Imaging
o Ultrasound - check for structural abnormalities
o CT/MRI
o X-Ray KUB - check for stones
• Renal Biopsy
Define epididymitis and orchitis
• Inflammation of the epididymis or testes
o 60% of epididymitis is associated with orchitis
o Most cases of orchitis are associated with epididymitis
Explain the aetiology/risk factors of epididymitis and orchitis
• Most cases are INFECTIVE in origin • Bacterial o If < 35 yrs: Chlamydia and Gonococcus o If > 35 yrs: mainly coliforms (e.g. Enterobacter, Klebsiella) o RARE: TB, syphilis • Viral o Mumps • Fungal o Candida if immunocompromised • 1/3 are IDIOPATHIC • Risk Factors o Diabetes o Rare: vasculitis (e.g. Henoch-Schonlein purpura)
Summarise the epidemiology of epididmytis and orchitis
- COMMON
- Affects all age groups
- Most commonly: 20-30 yrs
Recognise the presenting symptoms of epididymitis and orchitis
- Painful, swollen and tender testis or epididymis
- NOTE: less acute onset than testicular torsion
- Penile discharge
- IMPORTANT: ask about sexual history
Recognise the signs of epididymitis and orchitis on physical examination
- Swollen and tender epididymis or testis
- Scrotum may be erythematous and oedematous
- Pyrexia
- Walking will be painful
- Eliciting a cremasteric reflex may be painful
Identify appropriate investigations for epididymitis and orchitis
• Urine o Dipstick o Early morning urine collections for MC&S • Bloods o FBC - high WCC o High CRP o U&Es • Imaging o Increased blood flow on duplex examination
Generate a management plan for epididymitis and orchitis
• Medical o Antibiotics • Surgical o Exploration of testicles if testicular torsion cannot be excluded clinically o Required if an abscess develops
Identify possible complications of epididymitis and orchitis
- Pain
- Abscess
- Fournier’s gangrene (if the infection is left untreated and spreads)
- Mumps orchitis could cause testicular atrophy and fertility issues
Summarise the prognosis for patients with epididymitis and orchitis
- GOOD if treated
* May take up to 2 months for the swelling to resolve
Define glomerulonephritis
• An immunologically mediated inflammation of the renal glomeruli
Explain the aetiology / risk factors of glomerulonephritis
• There are loads of different types of glomerulonephritis with different aetiologies
• Some types are caused by the deposition of antigen-antibody complexes in the glomeruli
• This leads to inflammation and activation of complement and coagulation cascades
• The immune complexes may form within the glomerulus (more common) or be deposited from the circulation
• The antigens to which the antibodies are produced are UNKNOWN but may be associated with:
o Bacteria (e.g. Streptococcus viridans, Staphylococci)
o Viruses (e.g. HBV, HCB, measles, mumps, EBV)
o Protozoal (e.g. Plasmodium malariae, schistosomiasis)
o Inflammatory/Systemic diseases (e.g. SLE, vasculitis, cryoglobulinaemia)
o Drugs (e.g. gold, penicillinamine)
o Tumour
• Classification is based on the site of nephron pathology and its distribution
o Minimal-change Glomerulonephritis
• Light microscopy - minimal change
• Electron microscopy - loss of epithelial foot process
o Membranous Glomerulonephritis
• Thickening of glomerular basement membrane (GBM) from immune complex deposition
• Associated with Goodpasture’s Syndrome
o Membranoproliferative Glomerulonephritis (MPGN)
• Thickening of GBM
• Mesangial cell proliferation and interdeposition
o Focal segmental glomerulosclerosis
• Glomerular scarring
• Associated with HIV
o Focal segmental proliferative glomerulonephritis
• Mesangial and endothelial cell proliferation
• Focal = involvement of some glomeruli
• Segmental = involvement of parts of individual glomeruli
o Diffuse proliferative glomerulonephritis
• Same as above but affects ALL glomeruli
o IgA Nephropathy
• Mesangial cell proliferation
• Mesangial IgA and C3 deposits
o Crescentic Glomerulonephritis
• Crescent formation by macrophages and epithelial cells, which fills up Bowman’s space
o Focal Segmental Necrotising Glomerulonephritis
• Peripheral capillary loop necrosis (occurs in granulomatosis with polyangiitis, microscopy polyarteritis and other vasculitides)
• Often evolves into crescentic glomerulonephritis
NOTE: cryoglobulins are immunoglobulins that precipitate in the cold
Summarise the epidemiology of glomerulonephritis
• Accounts for 25% of the cases of chronic renal failure
Recognise the presenting symptoms of glomerulonephritis
- Haematuria
- Subcutaneous oedema
- Polyuria or oliguria
- History of recent infection
- Symptoms of uraemia or renal failure (acute and chronic)
Recognise the signs of glomerulonephritis on physical examination
• Hypertension
• Proteinuria
• Haematuria (especially in IgA nephropathy)
• Renal failure
• Nephrotic syndrome - consists of a TRIAD of:
o Proteinuria > 3.5 g/24 hrs
o Low serum albumin < 24 g/L
o Oedema
o NOTE: due to the hypoalbuminaema, the liver tries to compensate and increases production of lipids, causing hyperlipidaemia
• Nephritic syndrome (TRIAD: hypertension + proteinuria + haematuria)
o Syndrome comprising of signs of nephritis
o Pores in the podocytes are large enough to allow protein AND red blood cells to pass into the urine
o MAIN FEATURE: Haematuria
• This is in contrast to nephrotic syndrome, which is mainly concerned with proteinuria
o There may also be red cell casts in the urine - indicative of glomerular damage
o Other features:
• Proteinuria
• Hypertension
• Low urine output (due to decreased renal function)
o NOTE: in nephrotic syndrome, only PROTEINS are moving into the urine
Identify appropriate investigations for glomerulonephritis
• Bloods o FBC o U&Es + creatinine o LFTs (check albumin) o Lipid profile o Complement studies o Antibodies: • ANA • Anti-dsDNA • ANCA • Anti-GBM antibody • Cryoglobulins • Urine o Microscopy - check for red cell casts o 24 hr collection: creatinine clearance and protein • Imaging o Renal tract ultrasound to exclude other pathology (e.g. obstruction) • Renal Biopsy o For microscopy • Investigations for associated conditions (e.g. HBV, HCV and HIV serology)
