Renal & Urology Flashcards
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
What is amyloidosis?
A (heterogenous) group of diseases characterised by extracellular deposition of amyloid fibrils
What are the two main subtypes of amyloidosis?
Type AA: serum Amyloid A protein
-non-familial secondary amyloidosis: inflammatory polyarthropathies account for 60% of cases
Type AL: immunoglobulin light chain amyloidosis (primary amyloidosis)
Which are the main 2 organs affected by amyloidosis?
Kidneys
Heart
What is the epidemiology of amyloidosis?
In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually- RARE
What are the presenting symptoms of amyloidosis?
PMH of inflammatory conditions (RF) Chronic infections (RF) Positive FH (RF) Fatigue Weight loss Dyspnoea on exertion
What are the signs of amyloidosis on physical examination?
Jugular venous distension- high right-sided filling pressure
Lower extremity oedema (nephrotic syndrome)
Macroglossia- most specific finding for AL
Diffuse muscular weakness
Shoulder pad sign- psudeohypertrophy of amyloid
What are the appropriate investigations for amyloidosis?
1st line:
Serum/ urine immunofixation- presence of monoclonal protein
Immunoglobulin free light chain assay- diagnosing AL
Bone marrow biopsy- clonal plasma cells
Others:
Tissue biopsy, ECG (for conduction abnormalities)
What is bladder cancer?
Over 90% of cancers of the urinary bladder are urothelial carcinoma (previously termed transitional cell carcinoma)
What is associated with bladder cancer?
Smoking* Aromatic amines (rubber industry) Chronic cystitis Schistosomiasis (increases risk of squamous cell carcinoma) Pelvic irradiation
What is the aetiology of bladder cancer?
Smoking is the most important causative factor in bladder cancer, increasing the risk two- to fourfold
People with Type 2 DM
Chronic inflammation, Schistosoma infection, and chronic indwelling catheters increase the risk
What is the epidemiology of bladder cancer?
Bladder cancer ranks ninth in worldwide cancer incidence. >90% are transitional cell carcinomas (TCCS) in the UK
M:F is 5:2
What are the presenting symptoms of bladder cancer?
Painless haematuria
Recurrent UTIs
Dysuria: associated with aggressive bladder cancer
Voiding irritability
What are the appropriate investigations for bladder cancer?
Cystoscopy with biopsy is diagnostic* (camera imaging)
Urinalysis: haematuria, microscopy/cytology (cancers may cause sterile pyuria)
Renal and bladder ultrasound: bladder tumours and/or upper tract obstruction may be seen
CT urogram is both diagnostic and provides staging.
Bimanual examination under anaesthetic helps assess spread
MRI or lymphangiography may show involved pelvic nodes
Bloods: FBC (may be mildly anaemic), Alk Phos (may be elevated)
What is Chronic Kidney Disease (CKD)?
Defined by either a pathological abnormality of the kidney, such as haematuria and/or proteinuria, or a reduction in the glomerular filtration rate to <60 mL/min/1.73 m² for ≥3 months’ duration
(also known as chronic renal failure)
What is the aetiology of CKD?
The most common cause in the adult population is diabetes with hypertension as second
- Vascular disease: Hypertension, renal artery atheroma, vasculitis
- Glomerular disease: Glomerulonephritis, diabetes, amyloid, SLE
- Tubulointerstitial disease: Pyelonephritis/interstitial nephritis, nephrocalcinosis, tuberculosis
- Obstruction and others: Myeloma, HIV nephropathy, scleroderma, gout, renal tumour, inborn errors of metabolism (e.g. Fabrys disease)
- Congenital/inherited: Polycystic kidney disease, Alports syndrome, congenital hypoplasia
What is the epidemiology of CKD?
Common condition -often unrecognised until the most advanced stages
11% of the adult population worldwide has CKD
The incidence is rising and is thought to be due to an ageing population- a higher incidence of diseases such as diabetes and hypertension
What are the presenting symptoms of CKD?
Anorexia Nausea Malaise Pruritus (itchiness) Later: diarrhoea, drowsiness, convulsions, coma (Symptoms of the cause)
What are the signs of CKD on physical examination?
Systemic: -Kussmauls breathing: deep, labored breathing (acidosis) -Signs of anaemia -Oedema -Pigmentation -Scratch marks Hands: -Leuconychia (hypoalbuminaemia) Signs of complications (e.g. neuropathy, renal bone disease)
What are the appropriate investigations for CKD?
Serum creatinine: determine GFR: elevated: >97 micromol/L (>1.1mg/dL) in men; >105 micromol/L (>1.2 mg/dL) in women
Urinalysis: Haematuria and/or proteinuria, microalbuminuria (30 to 300 mg/day)
Renal Ultrasound: small kidney size (kidney atrophy), presence of obstruction/hydronephrosis, kidney stones
Renal Biopsy: determine underlying pathological diagnosis
Imaging: Signs of osteomalacia and hyperparathyroidism. CXR may show pericardial effusion or pulmonary oedema
Bloods:
-FBC (low Hb: normochromic, normocytic)
-U&E (low urea and creatinine)
-eGFR (can be derived from creatinine and age using the MDRD calculator)
-LowCa2+ , high phosphate, AlkPhos, PTH
What is a common complication of CKD?
Renal hyperparathyroidism-elevated parathyroid hormone levels secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D
What is Epididymitis and Orchitis?
Epididymitis is characterized by acute unilateral scrotal pain and swelling of less than 6 weeks’ duration.
The pain usually begins at the epididymis and can spread to the entire testicle (epididymo-orchitis)
What is the aetiology of Epididymitis and Orchitis?
- Among sexually active men of all ages, STI pathogens including Chlamydia trachomatis and Neisseria gonorrhoeaeare common causes of epididymitis
- In older men (>35 years), infection may be due to non-sexually transmitted infection with common uropathogens, such as Escherichia coli and Enterococcus faecalis
What is the epidemiology of Epididymitis and Orchitis?
Epididymitis is the most common cause of scrotal pain in adults with an incidence of 25–65 cases per 10,000 adult males per year
Over half of men and boys with epididymitis also have orchitis.
-Isolated orchitis is rare: the commonest cause is mumps infection, although it can also be caused by other viral infections
What are the presenting symptoms of Epididymitis and Orchitis?
Gradual onset (unlike testicular torsion)
Unilateral scrotal pain and swelling
Other symptoms: fever, dysuria
What are the signs of Epididymitis and Orchitis on physical examination?
Diffuse enlargement of the testis
Erythema of the scrotal skin
Swelling for < 6 weeks: otherwise indicates chronic inflammation
What are the appropriate investigations for Epididymitis and Orchitis?
*first catch urine sample
Urethral swab: highly sensitive and specific for documenting urethritis and the presence or absence of gonococcal infection (look for urethral discharge)
Urine dipstick test: positive leukocyte esterase test (urethritis and lower urinary tract infection)
Urine microscopy: WBC
Urine culture: isolate causative organism
Colour duplex ultrasound: done in patients with signs suggestive of abscess formation or possible testicular torsion and infarction; epididymis is enlarged and hyperaemic (increased blood flow)
Consider STI screen
What is the management for Epididymitis and Orchitis?
If <35yrs;
-Doxycycline 100mg/12h (covers chlamydia; treat sexual partners)
-If gonorrhoea suspected add ceftriaxone 500mg IM stat. If >35yrs (mostly non-STI) associated UTI is common:
-Ciprofloxacin 500mg/12h or ofloxacin 200mg/12h
*Antibiotics should be used for 2–4wks
Also: analgesia, scrotal support, drainage of any abscess.
What are the complications of Epididymitis and Orchitis?
(usually of chronic disease, more commonly associated with uropathogen enteric organisms than sexually transmitted organisms) include: Chronic pain Reactive hydrocele Abscess formation Infarction of the testicle Testicular atrophy Reduced fertility
What is the prognosis of Epididymitis and Orchitis?
In men with infectious acute epididymitis, symptoms usually resolve rapidly following the initiation of appropriate antibiotic therapy
RARE CASES: particularly in STIs-epididymal obstruction/testicular atrophy and subsequent infertility problems
What is glomerulonephritis?
Denotes glomerular injury and applies to a group of diseases that are generally characterised by inflammatory changes in the glomerular capillaries and the glomerular basement membrane (GBM)
What is the aetiology of glomerulonephritis?
There are many different types of glomerulonephritis with differing aetiologies. Some types of glomerulonephritis are ascribed to deposition of antigen–antibody immune complexes in the glomeruli that lead to inflammation and activation of complement and coagulation cascades. It is commonly idiopathic but there are other causes
What are some of the causes of glomerulonephritis?
- Infections (group A beta-haemolytic Streptococcus, respiratory and gastrointestinal infections, hepatitis B and C, endocarditis, HIV, schistosomiasis, malaria, and leprosy)
- Systemic inflammatory conditions such as vasculitides (SLE, rheumatoid arthritis, granulomatosis polyangiitis, microscopic polyangiitis and scleroderma)
- Drugs (penicillamine, gold sodium thiomalate, NSAIDS)
- Metabolic disorders (DM, hypertension, and thyroiditis)
- Malignancy (lung and colorectal cancer, melanoma, and Hodgkin’s lymphoma)
- Hereditary disorders (Alport’s syndrome, thin basement membrane disease and hereditary complement protein disorders)
- Deposition diseases (amyloidosis)
What is the epidemiology of glomerulonephritis?
Makes up to 25% of cases of chronic renal failure
