Haematuria (urology) Flashcards
(153 cards)
Define AKI
Sudden deterioration in kidney function
NICE specifications for presence of AKI
- urine output <0/5ml/kg for 6 hours
- > 50% rise in creatinine over 7 days
- 26 micromol rise in creatinine over 48 hours
Serum creatinine and urine output in AKI stage 1
Serum creatinine: 150-200% increase or 25 umol/l increase in 48h
Urine output: <0.5ml/kg/h for 6h
Serum creatinine and urine output in AKI stage 2
Serum creatinine: 200-300% increase
Urine output: 0.5 ml/kg/h for 12 h
Serum creatinine and urine output in AKI stage 3
Serum creatinine: >300% increase or >350umol/l with acute rise of >45umol/l in 48h
Urine output: <0.3ml/kg/h for 24h or anuria for 12h
What is pre-renal AKI
Occurs when the blood supply to the kidney is interrupted
2 causes:
- shock : hypovolemic, cardiogenic, distributive
- renovascular obstruction: aortic dissection, renal artery stenosis, ACEi
What is acute tubular necrosis
Prolonged interruption to the blood supply ischaemia leads to necrosis of the cells that line the renal tubules
- leads to porous tubular membranes and also blockage of the tubules by necroses cells
- urine is isotonic with plasma and has high sodium as concentrating powers are lost
What is post renal AKI
Occurs when there is obstruction to the outflow of the urinary tract
Leads to back flow of urine, damage to the kidney architecture and resultant organ failure
Blockage is often in the ureters
3 causes / mechanisms of renal AKI
Acute tubular necrosis (85%)
Interstitial nephritis (10%)
Glomerular disease (5%)
Causes of acute tubular necrosis
Drugs: aminoglycosides, cephalosporins, radiological contrast mediums, NSAIDs
Toxins: heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome
Pathophysiology of interstitial nephritis
Mainly caused by drugs
Damage is not limited to tubular cells and bypasses the BM to cause damage to the interstitium
- mainly caused by abx, diuretics, PPI, allopurinol
Management of interstitial nephritis
Withdrawal of the drugs and a short course of oral steroids
Anatomy of the glomerulus
3 layers for substances to pass through
1. Fenestrated capillary epithelium
2. BM
3. Visceral layer: formed by interdigitating podocytes
These create a sieve that allows small, charged ions through
Pathophysiology of glomerulonephritis
Antibody / T cell mediated immunological attack upon an antigen in the glomerulus which may be primary (always there) or secondary (acquired)
Examinations / investigations in AKI
Obs : hypotension = pre renal / hypertension = CKD
OE: palpable bladder = bladder outlet obstruction
Urine dip and MCS
Bloods
VBG /ABG: to assess acid / base status
ECG: hyperkalaemia
Renal USS: to look for post renal causes
Management of AKI
- Halt any damaging drugs eg ACEi / NSAIDs
- Treat pre renal causes with iv fluids
- Refer to urology to relieve obstruction
- Assess fluid status with volume replacement
Indications for acute dialysis
Refractory hyperkalaemia
Refractory acidosis
Pulmonary oedema
Uraemic pericarditis / encephalopathy
Causes of hyperkalaemia
AKI / CKD
Drugs: supplements, K sparing diuretics, ACEis, NSAIDs
Acidosis
Others: addisons / tumour lysis syndrome / burns
How does hyperkalaemia present on ECG
Tall, peaked T waves
Widened QRS complex
Flattened P waves / prolonged PR interval
What to do if there is >6.5mmol/L potassium or there are ECG changes
- Start continuous ECG monitoring
- 10ml of 10% calcium gluconate IV to stabilise myocardium (repeat at 5min intervals until a max of 3 doses)
- 50ml of 50% glucose with 10U ACTRAPID insulin into a large vein over 30mins to decrease K+ conc
- Consider 10mg salbutamol neb
- If pH <7.2 consider sodium bicarbonate IV if advised by renal reg
- Recheck K+ after 2 hours
- Calcium resonium can then be given orally / rectally - long term option
- Ensure underlying cause is being treated
What is benign prostatic hyperplasia
Benign nodular / diffuse proliferation of glandular layers of the prostate, leading to enlargement of the inner transitional zone
Affects 70% of those >70
BPH symptoms
Filling: urinary freq (nocturia), urinary urgency
Voiding: hesitancy, poor stream, post void dribbling, strangury, retention with overflow incontinence
Complications: haematuria, UTI, post renal aki
BPB investigations
PR: enlarged prostate, typically the sulcus is still palpable
Bloods: FBC, U&E, PSA
Urinalysis
Bladder USS
Transrectal USS
BPH complications
UTI
Overflow incontinence
Bladder calculi
Bladder diverticulae
Bilateral hydronephrosis and renal failure