GU Flashcards
(147 cards)
Define nephrolithiasis
Aka renal stones / renal coliculi / urolithiasis
Stones form when solutes leave the urine and crystallise
Where are stones usually formed in the body
Kidney
Ureter
Urethra
Bladder
What are renal stone precipitates most commonly formed from
Calcium oxalate
• Accounts for 90%
Its black/dark brown in colour —> radiopaque on X-ray (shows as a white spot) - as its absorbing more light
Types of stones formed
Calcium oxalate - most common
Calcium phosphate
Struvite (Risk factor for it - UTI)
Uric acid (urate) stones (Radiolucent on X-ray - transparent)
Cysteine
Risk factors for renal stones
Chronic dehydration
Hx of renal stones
Hypercalcaemia / hypercalciuria —> HyperPTH
Kidney disease —> Polycystic kidney disease
Foods —> chocolate, rhubarb, spinach, nuts
Are stones more common in men or women
Males
Sx for renal stones
Symptoms
• Severe flank pain - Loin to groin that is colicky - intermittent pain
• N & V
• Urinary urgency / frequency
• Haematuria - Micro / Macroscopic
• Fever - If suggests uric acid stone / pyelonephritis
Signs
• Flank/Renal angle tenderness
• Hypotensive & tachycardia
• Pyrexia - septic stone
Typical age for renal stone development
20-40 yrs old
Pathophysiology for renal stones
When excess solute or reduced solvent—> Supersaturated urine —> favours crystallisation—> stone leads to regular outflow obstruction—> Hydronephrosis
Dilation and obstruction in renal pelvis (increases damage + risk of infection)
Complication of renal stones
Hydronephrosis - AKI / renal failure
Urosepsis (Infection)
Recurrence of stone - very common
Investigation and Dx for renal stones
KUB X-ray - 1st line
Non-Contrast CT KUB - Gold standard and diagnostic!!!
DO NOT USE Contrast CT for suspected renal stones as it needs to be excreted —> harmful if theres an obstruction
Urinalysis - microscopic Haematuria ± pyuria if pyelonephritis is present
Bloods + U&Es
Tx for renal stones
< 5mm should pass
Symptomatic relief - IV fluids (hydrate) + Analgesia (Diclofenac - NSAID) - IV for severe pain
± Alpha 1 blocker (Tamsulosin) - helps with pain, not always used though
± Antibiotic for sepsis (Gentamycin - for pyelonephritis)
Surgery:
ESWL - extracarporeal shock wave lithotripsy
Breaks stones down with sound waves of stones 5-10mm / < 20mm
PCNL - Percutaneous nephrolithotomy
Keyhole removal of stones >20mm
If hydronephrosis - emergancy, so do Percutaneous nephrostomy
Commenest site of renal stone obstruction
PUJ - Pelvo-Uretric Junction (Distal i.e. ureter entering bladder point)
Pelvic brim - ureter crossover iliac vessel
VUJ - Vesico-uretric Junction (*proximal i.e. top of Exeter joining kidney)
What worsens renal stone pain
Diuretics + fluid
Define AKI
Acute drop in kidney function, characterised by:
Increased Creatinine & Urea
Decreased urine output
What is the diagnostic AKI criteria
RIFLE criteria used to detect AKI:
Increase in serum creatinine by ≥ 26 micromol/L within 48hrs
Increase in serum creatinine by ≥ 50% within past 7 days
(≥ 1.5x baseline serum creatinine in 7 days)
Decrease in Urine output by < 0.5mL / kg / hour for more than 6 hours
KDIGO criteria used for severity of AKI:
Stage 1 -
Rise in creatinine by ≥26.5 µmol/L … OR …
Rise in creatinine to 1.5-1.9x baseline … OR …
Fall in urine output to < 0.5 mL/kg/hour for ≥ 6 hours
Stage 2 -
Rise in creatinine to 2.0 to 2.9x baseline … OR …
Fall in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3 -
Rise in creatinine to ≥ 3.0 times baseline, or
Rise in creatinine to ≥353.6 µmol/L or
Fall in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, fall in eGFR to <35 mL/min/1.73 m2
Pathophysiology of AKI
Damage from AKI —> inability to remove toxins & regulate pH —> accumulation of the following:
K+ —> Hyperkalaemia - Arrhythmias
Urea —> Hyperuremia - Pruritus / Uremic frost
Fluid —> Oedema - Pulmonary ± peripheral oedema
H+ —> Acidosis
Causes of AKI
Whenever someone asks you the cause of renal impairment always answer “the causes are pre-renal, renal or post-renal”.
Pre-renal
Hypovolaemia - Dehydration / haemorrhage
Reduced cardiac output - Heart or liver failure / sepsis
Drugs - NSAIDS / ACEi / IV contrast
Renal
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Toxins (sepsis / ABx)
Post-renal
Obstructive uropathy - Renal stones / BPH
Drugs - Anticholinergics / CCBs
How can ACEi cause AKI
ACEi causes afferent arterioles constriction
Therefore reduced perfusion to kidney —> AKI
Pre-renal cause
Top 3 causes of AKI
Cardiogenic shock
Sepsis
Major surgery
Most common renal cause of AKI
Tubular - acute tubular necrosis
Px triad of: Fever, rash, eosinophilia
Risk factors for AKI
Increased age
Co-morbidities: HTN, chronic H.F, T2DM
Nephrotoxic drugs: NSAIDS, ACEi, ARBs, Gentmicin, IV contrast
Sepsis
Signs of AKI
Oedema:
Bibasal crackles,
Increased JVP,
Peripheral oedema
Palpable bladder
Hyperuremia
Uremic frost
Pruritis
Hyperkalaemia
Arrhthmias
Increased H+
Metabolic Acidosis
^ Px can present depending on the substances accumulated - Remember Pathophysiology
Signs of hypovolaemia
Dry mucous membranes
Decreased skin turgor
Reduced blood pressure
Sx of AKI
Reduced urine output ± urine colour change
Confusion / drowsiness
Dypnoea ± swollen ankle —> Oedema
Suprapubic pain —> Urinary retention
Haematuria —> Glomerulonephritis