Genitourinary Flashcards
What is nephrolithiasis?
- kidney stones
- slightly more common in men → testosterone = increased oxalate
What are kidney stones made of?
- calcium oxalate → radio-opaque
- uric acid → radio-lucent
- struvite → radio-opaque
- cystine
Risk factors for nephrolithiasis
- chronic dehydration
- obesity
- high protein/salt diet
- recurrent UTIs
- hyperparathyroidism → hypercalciuria
- congenital abnormalities
Presentation of nephrolithiasis
renal colic
- severe unilateral abdominal pain
- starts in loin, radiates to ipsilateral groin/testicle/labia
- sudden onset early in morning
- restlessness
- N&V
- haematuria
- dysuria
Investigations for nephrolithiasis
- dipstick → haematuria, leukocutes, nitrites
- bloods → FBC, CRP, U&E
GOLD STANDARD = non-contrast CT KUB
- US in pregnancy
- radio-opaque only visible on US
Management of nephrolithiasis
- symptomatic relief → hydration, NSAIDs, opioids
- small pass spontaneously
if too big:
- EWSL → break stone into smaller fragments using shockwaves
- uteroscopy
- PCNL → percutaneous access, use nephroscope to remove stone
lifestyle advice
- decrease Na and protein
- increase citrus fruit
- adequate fluid intake
When should treatment be provided immediately for nephrolithiasis?
- intolerable pain/vomiting
- signs of obstruction/infection/AKI
What are the functions of the kidney?
- water/hormone homeostasis
- waste/toxin removal
- RBC production
- activated vitD
Risk factors of CKD and AKI
- emergency surgery → risk of sepsis/hypovolaemia
- CVD risk
- diabetes
- HF
- age >65
- liver disease
- use of nephrotoxic drugs
Which drugs are nephrotoxic?
- NSAIDs
- aminoglycides
- ACEi
- ARBs
- loop diuretics
- metformin
- digoxin
- lithium
What is AKI?
- sudden decline in renal function
- determined by increased serum creatinine +/- decreased urine output
Causes of pre-renal AKI
- hypovolaemia secondary to D&V
- renal artery stenosis
Causes of intrinsic AKI
- glomerulonephritis
- acute tubular necrosis ATN
- acute interstitial nephritis AIN
- rhabdomyolysis
- tumour lysis syndrome
Causes of post-renal AKI
- kidney stone in ureter or bladder
- BPH
- external compression of ureter
Presentation of pre-renal AKI
- normal Na+
- raised urea and creatinine
- responds well to fluid therapy
Presentation of intrinsic AKI
- T1DM
- HTN
- low urine osmolality
- high urine Na+
- high blood K+
Presentation of post-renal AKI
- acute colicky pain radiating from loin to groin
- microscopic haematuria
Diagnosis of AKI
- rise in creatinine to 1.5-1.9 times baseline
- > 50% rise in creatinine over 7 days
- fall in urine output to less than 0.5 for >6hrs in adults (8hr in kids)
Management of AKI
- fluid balance
- remove nephrotoxic drugs
- treat hyperkalaemia → risk for arrythmia
- treat underlying cause
- RRT if no response to medical treatment
Complications of AKI
- end stage renal failure
- metabolic acidosis
- uraemia
- CKD
What is CKD
- abnormal kidney structure/function
- present for >3 months with implications for health
Causes of CKD
- diabetes
- HTN
- glomerulonephritis
- PDK
- VHL
- persistent pyelonephritis
- obstruction → stones, BPH, tumours
- nephrotoxic drugs
Presentation of CKD
- often asymptomatic until ESRF
- fluid retention → oedema, raised JVP
- oliguria
- uraemia → pruritus, uraemic frost, yellow-grey complexion, reduced appetite
- cardiac arrythymias
- fatigue
- pallor
- bone pain
Diagnosis of CKD
- eGFR <60
- eGFR <90, signs of renal damage
- albuminuria >30, albumin:creatinine >3