Renal and Urology Flashcards
Define acute kidney injury
Acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output. Can range from mild renal impairment to severe renal failure.
Explain the aetiology/risk factors of acute kidney injury
Pre-renal - reduced renal perfusion due to:
hypovolaemia (haemorrhage, severe vomiting)
Hypotension (sepsis, shock, anaphylaxis)
hypo-perfusion (renal stenosis, NSAIDs, ACEi, ARBs)
heart failure
third spacing of fluid (severe pancreatitis)
Renal - problems can occur in the tubules, glomerulus or interstitium:
acute tubular necrosis
glomerulonephritis
interstitial nephritis
Post renal - due to obstruction of urinary outflow tract: retroperitoneal fibrosis,
tumour
BPH
ascending urinary infection (pyelonephritis)
urinary retention
Summarise the epidemiology of acute kidney injury
Incidences of hospitalised patients range from 13-22%
Acute tubular necrosis (renal cause of AKI) accounts for 45-75% of AKI
ATN in ICU patients is cause by sepsis (pre-renal cause of AKI) in 35-55% of cases
Recognise the presenting symptoms of acute kidney
Presence of risk factors (advanced age, underlying kidney disease, malignant HTN, T2DM and exposure to nephrotoxins) oligourea (reduced urine output) Nausea and vomiting Dizziness confusion Orthopnoea Paroxysmal nocturnal dyspnoea
Recognise the signs of acute kidney injury on a physical examination
Hypertension
Dehydration leading to postural hypotension
Distended bladder
Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
Tachycardia
Orthostatic hypotension
Identify appropriate investigations for acute kidney injury and interpret the results
Basic metabolic profile (incl. urea and creatinine): elevated serum creatinine (this may be the only sign of a decline in renal function)
high serum potassium
metabolic acidosis
Ratio of serum urea to creatinine:
20:1 or higher supports pre-renal azotaemia
Urinalysis (MSU or clean catch specimen):
RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase (in cases of infection)
Urine culture:
bacterial or fungal growth may occur
FBC:
anaemia, leukocytosis, thrombocytopenia
Generate a management plan for acute kidney injury (pre-renal)
- volume expansion and/or RBC transfusion
with severe hypotension
2. vasopressor: dopamine 1mg/kg/min IV OR adrenaline 1mg/min IV
with fluid overload
3. diuretic: furosemide 20-40mg IV
with uraemia, metabolic acidosis, hyperkalaemia
4. renal replacement therapy
Generate a management plan for acute kidney injury (renal)
- treat underlying condition
with volume overload
2. diuretic: furosemide 20-40mg IV
with pre-existing pre-renal azotaemia
3. volume expansion: normal saline
- renal replacement therapy
Generate a management plan for acute kidney injury (post-renal)
- bladder catheterisation
- relief of obstruction above bladder neck
with volume overload
3. diuretic: furosemide 20-40mg IV
- renal replacement therapy
Identify the possible complications of acute kidney injury and its management
AKI: hyperphosphataemia uraemia volume overload (pulmonary oedema, peripheral oedema) hyperkalaemia metabolic acidosis end-stage renal disease
Summarise the prognosis for patients with acute kidney injury
In-hospital mortality rates associated with AKI vary from 6% to 80% Indicators of poor prognosis: Age Multiple organ failure Oliguria Hypotension CKD Patients who develop AKI are at increased risk of developing CKD
Define benign prostatic hyperplasia
slowly progressive nodular hyperplasia of the periurethral (transitional) zone of the prostate gland. This leads to prostatic enlargement and bladder dysfunction
It is the most frequent cause of LUTS in adult males
Explain the aetiology / risk factors of benign prostatic hyperplasia
Aetiology
age-related hormonal problems creating androgen/oestrogen imbalances.
Increases in prostatic stem cells.
Progression to pathological BPH to clinical BPH (when symptoms present) may require additional factors such as prostatitis, vascular effects and changes to the glandular corpuscle.
Risk factors
Age above 50 years and a positive family history
reduced risk with soya/vegetable based diets and negative association with cirrhosis
Summarise 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
Storage/Irritative symptoms:
frequency, urgency and nocturia
Voiding/Obstructive symptoms:
weak stream, hesitancy, intermittency, straining, incomplete emptying and post-void dribbling