Renal & Urology Flashcards
(144 cards)
What is benign prostatic hyperplasia?
Lower urinary tract symptoms (LUTS) caused by bladder outlet obstruction. There are two components:
- A static component related to an increase in benign prostatic tissue narrowing the urethral lumen
- A dynamic component related to an increase in prostatic smooth muscle tone mediated by alpha-adrenergic receptors
What is the aetiology of benign prostatic hyperplasia?
Hyperplasia of the epithelial and stromal compartments, particularly in the transitional zone, may be attributed to various factors including shifts in age-related hormonal changes creating androgen/oestrogen imbalances
What is the epidemiology of benign prostatic hyperplasia?
The prevalence of histological BPH increases with age, affecting approximately 42% of men between the ages of 51 and 60 years and 82% of men between the ages of 71 and 80 years
What are the presenting symptoms of benign prostatic hyperplasia?
Storage symptoms: -Frequency -Urgency -Nocturia Voiding symptoms: -Weak stream -Hesitancy -Intermittency -Straining -Incomplete emptying -Post-void dribbling
What are the signs of benign prostatic hyperplasia on physical examination?
Assess severity of symptoms and impact on life
PR exam: may demonstrate prostate volume ≥30 g, nodules or tenderness suspicious of prostate cancer or prostatitis
What are the appropriate investigations for benign prostatic hyperplasia?
MSU- urinalysis: pyuria (presence of pus)
Bloods: U&Es-kidney dysfunction
Ultrasound: hydronephrosis ( swollen kidney as the result of a build-up of urine), mass, urolithiasis (formation of stony concretions in the bladder or urinary tract)
Rule out cancer:
-PSA (prostate specific antigen): elevation greater than age guideline, non-specific for BPH
-Transrectal use and biopsy
What is the management for benign prostatic hyperplasia?
Main goal is to improve lower urinary tract symptoms (LUTS) in order to improve quality of life:
Lifestyle:
-Avoid caffeine, alcohol (to reduce urgency/nocturia)
-Relax when voiding and void twice in a row to aid emptying
-Control urgency by practising distraction methods (eg breathing exercises)
Medical therapy: (useful in mild disease, and while awaiting surgery)
-Alpha blockers are 1st line (eg tamsulosin 400mcg/d also alfuzosin, doxazosin, terazosin). Reduces smooth muscle tone (prostate and bladder)
-5 alpha-reductase inhibitors: can be added, or used alone, eg finasteride 5mg/d (reduce conversion of testosterone to the more potent androgen dihydrotestosterone)
Surgical therapy:
-Transurethral resection of prostate (TURP) ≤14% become impotent
-Transurethral incision of the prostate (TUIP) involves less destruction than TURP, and less risk to sexual function, gives similar benefit. Relieves pressure on the urethra. Maybe best surgical option for those with small glands <30g
- Retropubic prostatectomy is an open operation (if prostate very large)
-Transurethral laser-induced prostatectomy (TULIP) may be as good as TURP
-Robotic prostatectomy is gaining popularity as a less traumatic and minimally invasive treatment option
What are the complications of benign prostatic hyperplasia?
UTI Haematuria Bladder stones Acute urinary retention Renal insufficiency Sexual dysfunction Overactive bladder
What is the prognosis of benign prostatic hyperplasia?
The majority of patients with BPH can expect at least moderate improvement of their symptoms with a decreased bother score and improved quality of life
*some patients (20%) may still see a clinical progression For some the symptoms/ SE may affect sexual wellbeing including erectile function
What is acute kidney injury (AKI)?
An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output
What is the aetiology of acute kidney injury (AKI)?
AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease
What are the risk factors of acute kidney injury (AKI)?
Advanced age
Underlying kidney disease
Diabetes Mellitus
Sepsis- may result in acute tubular necrosis, infectious glomerulonephritis, pre-kidney AKI from hypotension, or drug-induced injury from medications
Nephrotoxins e.g. aminoglycosides, NSAIDs, vancomycin
What are the pre-renal causes of an AKI?
Reduced renal perfusion:
Shock (hypovolaemic, septic, cardiogenic)
hepatorenal syndrome (liver failure)
What are the renal causes of an AKI?
Acute tubular necrosis- ischaemia, drugs and toxins
Acute glomerulonephritis
Acute interstitial nephritis- NSAIDs, penicillins, sulphonamides
Vessel obstruction- Renal artery/vein thrombosis, cholesterol emboli, vasculitis
Other causes:
myeloma, haemolysis, nephropathy
What are the post renal causes of an AKI?
Stone
Tumour (pelvic, prostate, bladder)
Blood clots
Retroperitoneal fibrosis
What is the epidemiology of AKI?
Incidence of 1800 per million
What are the presenting symptoms of AKI?
Usually asymptomatic Lower urinary tract symptoms- urgency, frequency or hesitancy Low urine output (oliguria) Malaise Anorexia Nausea and vomiting Pruritus (itching) Drowsiness Convulsions, coma (caused by uraemia)
What are the signs of acute kidney injury (AKI) on physical examination?
Oedema
What are the appropriate investigations for AKI and interpret the results?
1st line:
Basic metabolic profile- an acutely rising creatinine may be the only sign. Acutely elevated serum creatinine, high serum potassium, metabolic acidosis.
Serum potassium- elevated in hyperkalaemia
LFTs will be deranged in hepatorenal syndrome
FBC- leukocytosis may suggest an infection
CRP- elevated in infection and vasculitis
Blood culture- Positive for bacterial pathogen
Urinalysis- RBCs, WBCs, cellular casts (glomerulonephritis), proteinuria, positive nitrite, and leukocyte esterase
CXR- signs of infection or fluid
ECG- changes associated with hyperkalaemia (tented T waves)
Others:
Renal ultrasound- check for an obstructive cause
What is the management plan for acute kidney injury?
1.Assess hydration and fluid balance:
Pulse rate, lying and standing BP, JVP, skin turgor, chest auscultation, peripheral oedema, central venous pressure, fluid and weight charts. ECG monitoring (hyperkalaemia)
- If hypovolaemic (+ hyperkalaemia)
- fluid resuscitation
- review medications and stop nephrotoxins
- identify and treat underlying cause
others:
- vasoactive drug
- blood transfusion - If hypervolaemic (+ pulmonary oedema and hyperkalaemia)
- loop diuretic (under specialist supervision) and sodium restriction
- identify and treat underlying cause
consider: renal replacement therapy
Metabolic acidosis (if pH < 7.2): 50–100 mL of 8.4% bicarbonate via central line over 15–30 min
What medications can cause an AKI?
Acute tubular necrosis (ATN): paracetamol, aminoglycosides, amphotericin B (anti-fungal), NSAIDs, ACE-inhibtors, lithium
Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides
Others: opioids, other antibiotics e.g. trimethoprim, vancomycin
What is the treatment for acute pulmonary oedema?
P- positioning (sit up)
O- oxygen
D- diuretic (furosemide) and fluid restriction
M- (dia)morphine
A- anti-emetics
N- nitrates (GTN infusion if SBP >110, or 2 puffs GTN spray if SBP >90)
What are the possible complications of acute kidney injury (AKI)?
Common and life-threatening: Hyperkalaemia Sepsis Metabolic acidosis Pulmonary oedema Hypertension. Less common: Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis
What is the prognosis for patients with acute kidney injury (AKI)?
Acute tubular necrosis has biphasic recovery starting with oliguria then leading to polyuria (resulting from regeneration of the tubular cells)
Prognosis depends on the number of other organs involved, e.g. heart, lung
Many of those with ATN recover
Acute cortical necrosis may cause hypertension and chronic renal failure