Uro/renal Flashcards
Benign Prostate Hyperplasia
Enlargement of the prostate.
C: Unknown. Function of 5a reductase increases with age which converts testosterone to DHT. DHT prevents apoptosis allowing continued cell growth.
Risk Factors = age, family history, Afro-Caribbean, obesity.
S: Either storage, voiding or mixture of symptoms.
Storage = frequency, nocturia, urgency, urgency with incontinence.
Voiding = hesitation, poor flow, incomplete emptying, terminal dribbling, straining.
Haematuria and dysuria are red flags. May have urinary retention.
D: Urinanlysis, DRE, urine flow study, Post void bladder scan, PSA, Transrectal ultrasound.
T: Advice - moderate caffeine and alcohol, train bladder. 1st line: alpha-blockers (e.g. Tamsulosin). 2nd line: 5a–reductase inhibitor (e.g. Finasteride).
Surgery includes TURP – transurethral resection of prostate, TUVP – transurethral electrovaporisation of prostate or open prostatectomy via abdominal or perineal incision.
Stress incontinence
Involuntary leakage on effort or exertion, or on sneezing or coughing.
C: Pelvic floor muscles and urethral sphincter becomes weak. Usually due to childbirth in women and damage to the bladder or surrounding area during surgery in men. Also due to neuro conditions like Parkinsons.
S: Involuntary urine leakage, vaginal bulge/pressure, urogenital atrophy.
D: Empty supine stress test - urine leakage, urinalysis, cough stress test - urine leakage, bladder diary.
T: Behavioural therapy. 1st line is alpha-agonist (pseudoephedrine) with adjunctive oestrogen if post-menopausal.
Urge incontinence
Involuntary leakage accompanied by, or immediately preceded by, a sudden compelling desire to pass urine which is difficult to defer (urgency).
C: Overactivity of detrusor muscles, comorbidities (type 2 diabetes, obesity, chronic UTIs), certain drugs (parasympathomimetics, antidepressants + hormone replacement therapy).
S: Involuntary urine leakage accompanied by or immediately preceded by urgency. Nocturia.
D: Empty supine stress test - urine leakage, Urinalysis, bladder diary.
T: 1st line = behavioural approaches and lifestyle changes (bladder retraining, pelvic muscle exercises, weight loss, caffeine reduction etc).
2nd line = pharmacotherapy - oxybutynin.
Prostate Cancer
Slow-growing tumour of the prostate gland.
C: Neoplasia of epithelial cells – mutation occurs in prostate cells which then avoid apoptosis and divide in uncontrolled way. Risk factors: increasing age, family history, Afro-Caribbean, Genetics, Diet (red meat).
S: Lower urinary tract symptoms (LUTS) including storage symptoms – frequency, nocturia, urgency +/- incontinence and voiding symptoms – hesitation, poor flow, incomplete emptying, terminal dribbling. Haematuria or erectile dysfunction, weight loss, sweating at night, fatigue, bone pain, anaemia.
D: DRE (firm/hard, asymmetrical, craggy or irregular), neuro exam, bladder palpation, bony tenderness, PSA, prostate MRI, Transrectal or Transperineal prostate biopsy.
T: Treatment depends on staging, grade, age, co-morbidities, life expectancy. Watchful waiting if low-risk. Radiotherapy – localized or locally advanced cancer.
Hormonal treatment (anti-androgen therapy). Surgery – total prostatectomy – used in localized prostate cancer <70.
Bladder cancer
A growth of abnormal tissue, known as atumour, develops in thebladderlining, may spread into the bladder muscle.
C: Smoking, second-hand smoke, occupational exposure to chemical carcinogens, such as aromatic amines and polycyclic aromatic hydrocarbons, exposure to drugs (e.g. phenacetin, cyclophosphamide), chronic inflammation.
S: Painless haematuria (either visible or non-visible), sometimes symptoms suggestive of a UTI (frequency, urgency, dysuria).
D: Urinalysis, cystoscopy, CT/MRI.
T: Transurethral resection of a bladder tumour (TURBT) and localised chemo for low-risk. At least 6 doses of chemotherapy using a catheter for intermediate risk. A second TURBT, a course of Bacillus Calmette-Guérin (BCG) treatment, and a cystectomy for high-risk. If muscle invasive, cystectomy or radiotherapy with adjunctive chemo.
Testicular cancer
Cancer develops in the testicular cells. Can be unilateral or bilateral. Good 5 year survival rate.
Germ cell tumours: Seminomas, Non-seminomas germ cell tumours, Embryonal carcinoma, Choriocarcinoma, Teratoma.
Gonadal stromal tumours: Sertoli cell, Leydig cell, Granulosa cell.
C: Unknown. Chromosome 12q mutations are usually present.
S: Painless/painful testis mass, lower abdo pain, increased size of testis, gynecomastia, metastasis evidence: dyspnoea, haemoptysis, palpable lymph nodes, bone pain
D: CXR, CT/MRI scan, ultrasound, elevated AFP and B-hCG in NSGCT, elevated lactase dehydrogenase in GCT.
T: Surveillance - Regular AFP/β-hCG serum-level monitoring, Chemotherapy, stem cell transplantation, surgery.
Acute glomerulonephritis
A specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage.
C: Usually post-infection with group A β-haemolytic streptococcus. Can also be caused by Staphylococcus, mumps, Legionella, hepatitis B and C, schistosomiasis, malaria. Can be associated with infective endocarditis, visceral abscess, SLE, shunt nephritis.
S: Haematuria (visible or non-visible), proteinuria, hypertension and oedema, Oliguria, Uraemia (high urea).
D: Urinalysis, FBC, U&Es, immunology (anti-GBM, ANCA, ANA, complement levels), biopsy, ultrasound, CXR, CT scan, intravenous pyelogram.
T: Spontaneous recovery should take place. Hypertension is treated with salt restriction, loop diuretics and vasodilators.
Fluid balance is monitored by daily weighing and daily recording of fluid input and output.
IgA nephropathy
Abnormal IgA forms and deposits in the kidneys, causing kidney damage.
C: Abnormal glycosylation of the serine and threonine residues, causing IgAs to be galactose deficient. They are not recognised and not degraded, allowing them to accumulate, and IgG are produced against them. Typically develops during an infection in the mucosal lining, like infections of the gastrointestinal or respiratory tract.
S: Microscopic or gross haematuria, urine shows erythrocytes, casts and proteinuria, AKI or CKD, loin pain.
D: Urinalysis, urine microscopy, 24 hours of protein excretion, U&Es, creatinine and a 24-hour creatinine clearance test, plama IgA (poor test).
T: No cure but prevent further damage. Control blood pressure - good diet, low salt and cholesterol, antihypertensives.
Corticosteroids like prednisone, prevents the production of IgA1 and anti-glycan IgG
Nephrotic syndrome
Increased filtration of macromolecules across the glomerular capillary wall due to structural and functional damage of the basement membrane.
C: Primary - Minimal change glomerular disease, Focal segmental glomerulosclerosis and membranous glomerulonephritis,
Secondary - infection, SLE, RA, polyarteritis nodosa, DM, hereditary nephritis, sickle cell disease, malignancy, medications, toxins, pregnancy, transplant rejection.
S: Peripheral oedema usually ankles and legs but can progress, frothiness of their urine, arterial or venous thromobosis, recurrent infections and/or general fatigue, lethargy, poor appetite, weakness, breathlessness, dyslipidaemia: eruptive xanthomata, xanthelasmata.
D: Urinalysis, MSU, urinary protein:creatinine ratio, FBC, coag, U&Es, ESR, CRP, autoimmune screen, fasting glucose, CXR and abdominal or renal ultrasound scan, biopsy.
T: Sodium and fluid restriction and high-dose diuretic treatment - furosemide (~1 mg/kg/day) ± spironolactone (~2 mg/kg/day). Check weight regularly. Corticosteroids in children. ACEi may be used in adults.
Minimal change disease
Most common nephrotic disease in children. The glomeruli are damaged and become more permeable, allowing plasma proteins into the nephron and the urine, causing proteinuria. The damage can only be seen under an electron microscope.
C: In adults it’s usually secondary. In children it’s usually idiopathic or caused by allergic reactions, NSAIDs, tumours, viral infections.
S: Foamy urine, oedema, weight gain, nephrotic syndrome (proteinuria, oedema, hypoalbuminemia, dyslipidemia).
D: Urinalysis, FBC, eGFR, kidney biopsy.
T:Salt and fluid restriction, diuretics, ACEi/ARB, corticosteroids (prednislone). If steroid-resistent, levamisole, alkylating agents, calcineurin inhibitors, antiproliferatives, and rituximab.
Erectile dysfunction
Unable to develop or maintain an erection during sex.
C: Psychological - stress, performance anxiety, depression, physiological - atherosclerosis, blood vessel damage due to HTN or DM, stroke, multiple sclerosis, back or pelvis trauma can directly damage the nerves, hypogonadism, Peyronie’s disease, medication side-effects (diuretics, antidepressants, methadone).
S: Difficulty developing or maintaining an erection, decreased libido, may have premature or delayed ejaculation, anorgasmia.
D: HbA1c, morning sample of total testosterone, FSH, LH, rigidity studies, vascular studies (duplex ultrasound), neurological studies, endocrine work-up,psychodiagnostic evaluation.
T: PDE-5 inhibitors (sildenafil) - inhibit the PDE-5 enzyme in endothelial cells (normally breaks down cGMP), leading to higher levels of cGMP, leading to more smooth muscle relaxation
Vacuum erection device - applying negative pressure around the penis, which can help draw in blood
Prosthetic implants - can keep the penis rigid.
Priapism
Involuntary, persistent erection unrelated to sexual stimulation and unresolved by ejaculation.
C: Often idiopathic, Low flow - Hypercoagulable state (sickle cell anaemia, anaemia, thalassemia), Neurological disease (spinal cord stenosis), Metastatic disease (prostate cancer, bladder cancer), Medication relaxing smooth muscles (prostaglandins, hydralazine), High flow - Penile/perineum trauma (artery rupture, fistula).
S: Persistent erection lasting 30 minutes to 3 hours. Low flow - painful, corporeal aspiration (dark blood).
D: Doppler ultrasound, CT scan, Penile blood gas measurement, FBC, Selective angiography.
T: Low flow - intracavernosal injection of sympathomimetic agent e.g. phenylephrine (pure alpha agonist effects)
Treat underlying condition
Corporal aspiration with/without saline irrigation
High flow - identification, obliteration of fistulas with selective arterial embolisation
Chronic kidney disease
Subtle decline in function that develops over a minimum of 3 months.
C: Hypertension, DM, SLE, RA, HIV, NSAIDs and other medications, toxins like tobacco.
S: Ureamia, loss of appetite and nausea, encephalopathy which leads to asterixis, pericarditis, bleeding, Uremic frost (uric crystals in skin), hyperkalaemia and cardiac arrythmias, hypocalcaemia and renal osteodystrophy, hypertension.
D: Changes in GFR over time - may be suspected if GFR is less than 90ml/min/1.73m2
Irreversible kidney damage is diagnosed if the GFR is less than 60ml/min/1.73m2
Biopsy - look for glomerulosclerosis
T: Managing the underlying cause. Dialysis. Kidney transplant.
Urinary tract infections
Bacteria typically enter the bladder through the urethra.
C: Commonly E.coli, can also be caused by Proteus, Klebsiella, Enterococci, Staph.saprophyticus, S.aureus, Pseudomonas aeruginosa.
More common in women, the elderly, hospitalised patients, patients using a catheter, new sexual activity.
S: Lower UTI: frequency of micturition, dysuria, suprapubic pain and tenderness, haematuria and smelly urine.
Upper UTI (acute pyelonephritis): loin pain and tenderness, nausea, vomiting, fever.
Can be asymptomatic. New confusion in the elderly.
D: Uncomplicated UTIs in younger women with 2 of the 3 (dysuria, urgency or frequency) can be treated without diagnostic tests.
Otherwise, urinalysis and MSU culture.
T: Antibiotics for uncomplicated (3 days) and complicated (7 days).
Lower: Trimethoprim–sulfamethoxazole or nitrofurantoin.
Upper: Antibiotics are given intravenously, e.g. aztreonam, cefuroxime, ciprofloxacin or gentamicin, switching to a further 7 days oral treatment as symptoms improve.
Fluid intake and hygiene advice.
Acute pyelonephritis
Inflamed kidney that develops relatively quickly, usually a result of a bacterial infection. Type of upper UTI.
C: Most commonly caused by ascending infection from the lower urinary tract. E.coli, Proteus and Enterobacter. Commonly found in the bowel flora.
Haematogenous infection can also occur from septicaemia or infective endocarditis.
S: Leucocytosis, fevers, chills, nausea and vomiting, flank pain at the costovertebral angle, systemic symptoms help distinguish from a lower UTI.
D: Urinalysis, MSU culture, CRP, ESR, FBC, blood cultures, Ultrasonography, Contrast-enhanced helical/spiral CT, renal biopsy, MRI scan.
T: Fluid intake, analgesia, first-line antibiotic should be either ciprofloxacin or co-amoxiclav for seven days, Trimethoprim may be used if culture confirms sensitivity. Surgery may be used to drain renal or perinephric abscesses.