10. GU Flashcards
what r nephroliathiasis and what are they made of and where do they form
kidney stones
calcium oxolate
collecting duct
explain the pathophysiology of nephroliathiasis
- excess solute in collecting ducts leads to crystallisation of urine
- these obstruct the outflow of urine
what is a complication of nephroliathiasis and explain what this is and how this this treated
hydronephrosis- dilation of the renal pelvis in response to obstruction
surgical decompression
what 2 risks increase with obstruction and dilation of the renal pelvis
- infection risk
- obstruction causes prostaglandin release which results in natural diuresis risk
what r the 3 most common obstruction sites for nephroliathiasis
- PUJ pelvo-ureteric junction
- pelvic brim (where ureter crosses over iliac blood vessels)
- VUJ vesico-urethral junction
presentation of nephroliathiasis 4
- unilateral, colicky pain from loin to groin which comes in peristaltic waves
- patient cannot lie still
- haematuria
- dysuria
1st line and GS/ diagnostic for nephroliathiasis and give their pros and cons (2, 3)
1st line: kidney, ureter and bladder X ray
-> 80% specific for stones
-> cheap and easy
GS: Non contrast CT KUB -> 90% specific for stones
-> rapid
-> background radiation
with urinary symptoms what test is important to take if the presenting patient is female
pregnancy test
treatment of nephrothialiasis 4
- watch and wait for stones smaller than 5mm as they spontaneously pass
- medium stones require either endoscopic sound wave lithotripsy (breaks up the stones)
- large stones require percutaneous nephrolitherectomy (keyhole surgery)
- analgesia- IV diclofenac
what is acute kidney injury and what 3 things characterise it
abrupt decline in kidney function (hours-days)
1. increased serum creatinine
2. increased urea
3. decreased urine output
explain the classification criteria for acute kidney injury 3
KDIGO:
1. serum creatinine above 26 micromol/L within 48 hours - needs a baseline
OR
2. 1.5 times the baseline in 7 days (increase of 50%)
3. urine output <0.5ml/kg/hour for 6 or more consecutive
how to determine the type of acute kidney injury 1 and what value determines each type 3
urea: creatinine ratio
>100:1= pre renal
<40:1= renal
40-100= post renal
what is the staging method for acute kidney injury, what r the stages and what does a higher stage mean
AKIN
stage 1-3
higher stage= decreased likelihood of kidney recovery
what r the top 3 causes of AKI
sepsis, cardiogenic shock, MAJOR SURGERY
what are the 4 pre renal causes of AKI and what is the general trend
- decrease in CO: heart failure or shock
- liver failure
- renal artery stenosis
- drugs: NSAIDs, ACEi, IV contrast
-> all to do with hypoperfusion
what are the 4 renal causes of AKI and what is the general trend
- tubular (acute tubular necrosis)
- interstitial
- glomerular (inflammation)
- toxins (sepsis)
-> nephron and parenchyma damage
what r the 3 post renal causes of AKI and what is the general trend
- stones (ureteral, bladder or urethra)
- BPH
- drugs (ANTICHOLINERGICS, calcium channel blockers)
-> obstructive uropathy
risk factors of AKI 2
elderly
nephrotoxic drugs
which substances accumulate due to AKI 4 and what do they lead to 4
K+= arrythmias
H+= acidosis
urea= pruritis due to urea deposites in the skin
fluid= odema
symptomatic presentation of AKI 3
- oedema- swelling of limbs and abdomen
- oligouria/ haematuria/ proteinuria (changes to urine)
- ENCEPHALOPATHY/ MENTAL CONFUSION
investigations for AKI 1 AND 2 WAYS OF DETERMINING CAUSES
- establish cause with urea: creatinine ratio
- FBC: K+, H+, urea and creatinine
- RENAL CAUSE- RENAL BIOPSY
- POST RENAL- KUB US
treatment of AKI 3 and what is the last resort treatment
treat complications:
1. high K+- calcium gluconate
2. metabolic acidosis- sodium bicarbonate
3. oedema= diuretics
last resort= renal replacement therapy
what indicates haemo-dialysis in AKI 5
Acidodid (pH <7.1)
Fluid overload (odema)
Uremia (symptomatic)
K+ >6.4
ECG changes due to K+
AFUKE
what is CKD
eGFR of <60mL/min/1.73m2 for 3 or more months