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Year 3 ICSM Sofia > Renal & Urology > Flashcards

Renal & Urology Flashcards

1
Q

What is acute kidney injury?

A

An acute decline in the GFR from baseline, with or without oliguria/anuria

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2
Q

What is the aetiology of acute kidney injury?

A

Pre-renal:
- Various causes of reduced renal perfusion such as hypovolaemia, haemorrhage, sepsis, third spacing of fluid (e.g. severe pancreatitis), overdiuresis, heart failure
Intrinsic:
- Acute tubular necrosis, rapidly progressive glomerulonephritis, interstitial nephritis
Post-renal:
- Mechanical obstruction of the outflow tract. Retroperitoneal fibrosis, lymphoma, tumour, prostate hyperplasia, strictures, renal calculi, ascending urinary infection and urinary retention

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3
Q

What is the epidemiology of acute kidney injury?

A
  • Rate of hospitalisation for kidney disease has increased, particularly amongst adults over 65
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4
Q

What are the risk factors for acute kidney injury?

A
  • Advanced age
  • Underlying renal disease
  • Malignant hypertension
  • Diabetes mellitus
  • Myeloproliferative disorders e.g. multiple myeloma
  • Connective tissue disease
  • Trauma
  • Haemorrhage
  • Exposure to nephrotoxins
  • Sepsis
  • Pancreatitis
  • Drug overdose
  • Surgery
  • Recent vascular intervention
  • Excessive fluid loss
  • Nephrolithiasis
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5
Q

What are the presenting symptoms of acute kidney injury?

A
  • Reduced urine production
  • Vomiting
  • Dizziness
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Seizures
  • Fever
  • Haematuria
  • Rash
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6
Q

What are the signs of acute kidney injury on examination?

A
  • Pulmonary oedema
  • Tachycardia
  • Orthostatic hypotension
  • Hypertension
  • Peripheral oedema
  • Muscle tenderness
  • Limb ischaemia
  • Prostatic obstructive symptoms
  • Arthralgia/arthritis
  • Altered mental status
  • Signs of uraemia
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7
Q

What are the investigations for acute kidney injury?

A
  • Basal metabolic profile (including urea & creatinine): Acutely elevated serum creatinine, high serum potassium, metabolic acidosis
  • Ratio of serum urea to creatinine: 20:1 or higher supports pre-renal azotaemia
  • Urinalysis: RBCs, WBCs, cellular casts, proteinuria, bacteria, positive nitrite and leukocyte esterase
  • Urine culture: Bacterial or fungal growth may occur
  • FBC: anaemia, leukocytosis, thrombocytopenia
  • Renal US: Dilated renal calcyces
  • CXR: pulmonary oedema, cardiomegaly
  • ECG: Peak T waves, increased PR interval, widened WRS, atrial arrest and deterioration to a sine wave pattern (if severe hyperkalaemia)
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8
Q

How is acute renal injury managed?

A
  • Volume expansion and/or RBC transfusion
  • Vasopressor
  • Diuretic
  • Renal replacement therapy
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9
Q

What are the possible complications of acute renal injury?

A
  • Hyperphosphataemia
  • Uraemia
  • Volume overload
  • Hyperkalaemia
  • Metabolic acidosis
  • Chronic progressive kidney disease
  • End-stage renal disease
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10
Q

What is the prognosis of acute renal injury?

A
  • Variable, depends on cause of injury and severity and duration of AKI
  • Up to 6% of patients admitted to ICU have AKI requiring renal replacement therapy (RRT). In hospital, when AKI requires dialysis, mortality exceeds 50%, especially in those with multiorgan failure. Mortality rates are high due to death from underlying disease and complications, not just the AKI.
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11
Q

What is benign prostatic hyperplasia?

A

A noncancerous increase in the size of the prostate
- Involves hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the transition zone of the prostate

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12
Q

What is the aetiology of benign prostatic hyperplasia?

A
  • Hyperplasia of epithelial and stromal compartments, may be attributed to various factors including shifts in age-related hormonal changes creating androgen/oestrogen imbalances
  • Progression from pathological BPH to clinical BPH may require additional factors such as prostatitis, vascular effects and changes in the glandular capsule
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13
Q

What is the epidemiology of benign prostatic hyperplasia?

A

Prevalence of histological BPH does increase with age and affects approximately 42% of men between the ages of 51 and 60 years, and 82% of men between the ages of 71 and 80 years.

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14
Q

What are the presenting symptoms of benign prostatic hyperplasia?

A
  • Presence of risk factors (over 50yrs)
  • Storage symptoms: Frequency, urgency, nocturia
  • Voiding symptoms: Weak stream, hesitancy, intermittency, straining, incomplete emptying and post-void dribbling
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15
Q

What are the signs of benign prostatic hyperplasia on examination?

A
  • Bladder enlargement on abdo exam

- Rectum exam: enlarged prostate feels smooth, cannot obtain accurate representation of prostate size

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16
Q

What are the investigations for benign prostatic hyperplasia?

A
  • MSU, U&Es
  • Ultrasounds: large residual volume-?hydronephrosis
  • Rule out cancer: transrectal USS, biopsy, PSA
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17
Q

How is benign prostatic hyperplasia managed?

A
  • Lifestyle: Reassure against prostate cancer, avoid caffeine and alcohol, drink less at night, relax when voiding, voiding twice in a row to aid emptying, control urgency by practicing distracting methods, train bladder to hold on
  • Mild to moderate: watchful waiting
  • Moderate: alpha blockers (decrease smooth muscle tone of prostate and bladder). Competitive inhibitor of 5a-reductase (finasteride)
  • Surgery: when decreased renal function and upper tract dilation
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18
Q

What are the possible complications of benign prostatic hyperplasia?

A

Acute retention/retention with overflow

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19
Q

What is the prognosis for benign prostatic hyperplasia?

A

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. L

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20
Q

What is chronic kidney disease?

A

Defined either as kidney damage or GFR of less than 60mL/min/1.73m2 for 3 months
- Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies

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21
Q

What is the aetiology of chronic kidney disease?

A
  • Diabetes mellitus and hypertension are two most common causes
  • 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. Fabry’s disease)
  • Congenital/inherited: Polycystic kidney disease, Alport’s syndrome, congenital hypoplasia
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22
Q

What is the epidemiology of chronic kidney disease?

A
  • Incidence of end stage CKD in England more than 110 per million population per year
  • Higher incidence in Asian immigrants than native British population
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23
Q

What are the presenting symptoms of chronic kidney disease?

A
  • Anorexia, nausea, pruritis
  • Later: diarrhoea, drowsiness, convulsions, coma
  • Symptoms of cause and other complications
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24
Q

What are the signs of chronic kidney disease on examination?

A
  • Systemic: Kussmaul’s breathing (acidosis), signs of anaemia, oedema, pigmentation, scratch marks
  • Hands: Leuconychia, brown line at distal end of nail
  • May be an arteriovenous fistula (buzzing lump in wrist or forearm)
  • Signs of complications (e.g. neuropathy, renal bone disease)
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25
Q

What are the investigations for chronic kidney disease?

A
  • Blood: FBC (decreased Hb: normochromic, normocytic) U&E (decreased urea and creatinine), eGFR (can be derived from creatinine and age using the MDRD calculator), decreased Ca++. raised phosphate, AlkPhos, PTH
  • Investigate for suspected aetiology e.g. ANCA, ANA, glucose
  • 24h urine collection: Protein, creatinine clearance (which is rough estimate of GFR)
  • Imaging: Signs of osteomalacia & hyperparathyroidism. CXR may show pericardial effusion or pulmonary oedema
  • Renal ultrasound: Measure size, exclude obstruction and visualise structure
  • Renal biopsy: For changes specific to underlying disease, contraindicated for small kidneys
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26
Q

What is epididymitis and orchitis?

A

Epididymitis: Infection or less frequently, inflammation of epididymis (coiled tube on back of testicle
Orchitis: Inflammation of one or both of the testicles

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27
Q

What is the aetiology of epididymitis and orchitis?

A
  • Chlamydia (under 35 yrs)
  • E. coli
  • Mumps
  • N. Gonorrhoea
  • TB
  • Non-STI (associated with UTI) if over 35 yrs
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28
Q

What is the epidemiology of epididymitis and orchitis?

A

Fifth most common urological diagnosis in men ages 18-50 years

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29
Q

What are the presenting symptoms of epididymitis and orchitis?

A
  • Sudden onset tender swelling
  • Dysuria
  • Sweats/fever
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30
Q

What are the signs of epididymitis and orchitis on examination?

A
  • Parotid swelling (RNA paramyxovirus) if Mumps
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31
Q

What are the investigations for epididymitis and orchitis?

A
  • First catch urine sample
  • Urethral discharge swab -> MC & S
  • STI screen
  • Warn of possible infertility, Sx getting worse before improvement
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32
Q

How is epididymitis and orchitis managed?

A
  • If under 35 yrs, Doxocycline or azithromycin (chlamydia, trachomatis, STI), Rx sexual partners, Cetriaxone is neisseria gonorrheae suspected
  • Over 35: Ciprofloxacin
  • Analgesia, scrotal support, abscess drainage
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33
Q

What are the possible complications of epididymitis and orchitis?

A
  • Scrotal abscess and pyocele
  • Testicular infarction
  • Fertility problems
  • Testicular atrophy
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34
Q

What is the prognosis of epididymitis and orchitis?

A

Patients with epididymitis secondary to a sexually transmitted disease have 2-5 times the risk of acquiring and transmitting HIV.

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35
Q

What is glomerulonephritis?

A

Immunologically mediated inflammation of renal glomeruli?

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36
Q

What is the aetiology of glomerulonephritis?

A

Infection: Bacterial (streptococcus viridans, group A B-haemolytic streptococci, staphylococci, gonococci, Salmonella, syphillis) Viral (Hep B/C, HIV, measles, mumps, ECV, VZV, coxsackie) Protozoal (Plasmodium malariae, schistosomiasis, filariasis

  • Inflammatory/systemic diseases: SLE, systemic vasculitis, cyroglobulinaemia
  • Drugs: Gold, penicillamine
  • Tumours: Classified based on site of nephron pathology and its distribution
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37
Q

What is the epidemiology of glomerulonephritis?

A

Makes up to 25% of cases of chronic renal failure

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38
Q

What are the presenting symptoms of glomerulonephritis?

A
  • Heamaturia, subcutaneous oedema, polyuria or oliguria, proteinuria. History of recent infection
  • Symptoms of uraemia or renal failure (acute and chronic)
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39
Q

What are the signs of glomerulonephritis on examination?

A
  • Hypertension
  • Proteinuria (less than 3g/24h)
  • Haematuria (microscopic or macroscopic, especially IgA nephropathy)
  • Nephrotic syndrome (usually for minimal-change glomerulonephritis in children and membranous glomerulonephritis in adults)
  • Nephritic syndrome (haematuria, proteinuria, subcutaneous oedema, oliguria, hypertension, uraemia)
  • Renal failure (acute or chronic) and
  • Partial lipodystrophy (loss of subcutaneous fat in MPGN type II)
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40
Q

What are the investigations for glomerulonephritis?

A
  • Blood: FBC, U&E and creatinine, LFT (albumin), lipid profile, complement studies (C3,C4, C3 nephritic factor in MPGN), ANA, anti-double stranded DNA, ANCA, anti-GBM antibody, cyroglobulins if appropriate
  • Urine: Microscopy (dysmorphic RBCs, red-cell casts, 24h collection, creatinine clearance, protein
  • Imaging: Renal tract ultrasound (to exclude other pathology)
  • Renal biopsy: Light microscopy, electron microscopy, immunofluorescence microscopy
  • Investigation for associated infections e.g. Hep B, Hep C or HIV serology
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41
Q

What is hydrocele?

A
  • Collection of serous fluid between layers of membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord.
  • Communicating and non-communicating
  • In communicating hydroceles, a patent processus vaginalis connects the peritoneum with the tunica vaginalis, which allows peritoneal fluid to flow freely between both structures
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42
Q

What is the aetiology of hydrocele?

A
  • Most paediatric hydroceles are congenital and resolve within the first year of life in the majority of cases
  • Most adult hydroceles are acquired
  • Non-communicating hydroceles found secondary to minor trauma, infection, testicular torsion, epididymitis, varicele operation or testicular tumour
  • Communication hydroceles may occur following icnreased intra-abdominal fluid or pressure (due to shunts, peritoneal dialysis, or ascites) if there is a patent processus vaginalis
  • Pts with connective tissue disorders have high risk of communicatin hydroceles
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43
Q

What is the epidemiology of hydrocele?

A
  • Predonominantly occur in males, rare in females

- They are common in male infants and children and in many cases are associated with an indirect inguinal hernia

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44
Q

What are the presenting symptoms of hydrocele?

A
  • Presence of risk factors: Male sex, prematurity & low birth weight
  • Infants
  • Scrotal mass
45
Q

What are the signs of hydrocele on examination?

A
  • Transillumination
  • Enlargement of scrotal mass following activity
  • Variation in scrotal mass during the day
46
Q

What are the investigations for hydrocele?

A
  • Clinical diagnosis

- Ultrasound

47
Q

What is nephrotic syndrome?

A

Characterised by proteinuria (over 3g/24h), hypoalbuminaemia (less than 30g/L), oedema and hypercholesterolaemia

48
Q

What is the aetiology of nephrotic syndrome?

A

Commonest cause in minimal change in glomerulonephritis in children but all forms of glomerulonephritis can cause nephrotic syndrome
- Other causes: diabetes mellitus, sickle cell disease, amyloidosis, malignancies (lung and GI adenocarcinomas), drugs (NSAIDs), Alport’s syndrome, HIV infection

49
Q

What is the epidemiology of nephrotic syndrome?

A
  • Most common cause in children (90%): minimal change glomerulonephritis (usually seen in boys under 5yrs, rare in black populations)
  • Most common causes in adults: diabetes mellitus, membranous glomerulonephritis
50
Q

What are the presenting symptoms of nephrotic syndrome?

A
  • Family history of atopy in those with minimal change glomerulonephritis, family history of renal disease
  • Swelling of face, abdomen, limbs, genitalia
  • Symptoms of underlying cause (e.g. SLE)
  • Symptoms of complications (e.g. renal vein thrombosis: loin pain, haematuria)
51
Q

What are the signs of nephrotic syndrome on examination?

A
  • Oedema: peiorbital, peripheral, genital

- Ascites: fluid thrill, shifting dullness

52
Q

What is the pathogenesis of nephrotic syndrome?

A

Structural damage to basement membrane or reduction in negatively charged components within it reduces the filtration of large protein molecules by the glomerulus, causing proteinuria and hypoalbuminaemia

53
Q

What are the investigations for nephrotic syndrome?

A
  • Blood: FBC,U&E, LFT (decreased albumin), ESR/CRP, glucose, lipid profile (secondary hyperlipidaemia, immunoglobulin
54
Q

What are the tests to identify the underlying cause of glomerulonephritis (used for nephrotic syndrome)?

A
  • SLE: ANA, anti-dsDNA
  • Infections: Group A B-haemolytic streptococcal infection (ASO titre, HBV infection (serology), plasmodium malariae (blood films)
  • Goodpasture’s syndrome: Anti-glomerular basement membrane antibodies
  • Vasculitides: e.g. Wegener’s and microscopies polyarteritis (ANCA)
  • Urine: Urinalysis, microscopy
  • Renal ultrasound: Excludes other renal disease that may cause proteinureia e.g. reflux nephropathy
  • Renal biopsy
  • Other imaging: Doppler, renal angiogram
55
Q

What is polycystic kidney disease (PKD)?

A

Autosomal dominant inherited disorder characterised by the development of multiple renal cysts that gradually expand and replace normal kidney substance, variably associated with extrarenal (liver and cardiovascular) abnormalities

56
Q

What is the aetiology of polycystic kidney disease?

A
  • 85% are mutations in PKD1 on chromosome 16, a membrane bound multidomain protein involved in cell-cell and cell-matrix interactions: 15% are mutations in PKD2 on chromosome 4, a Ca++ permeable cation channel
  • Pathological process is considered to be a proliferative/hyperplastic abnormality of the tubular epithelium. In early stages, cysts are connected to the tubules from which they arise and the fluid content is glomerular filtrate. When cyst diameter >2mm, most detach from the patent tubule and fluid content is derived from secretions of the lining epithelium. With time, cysts enlarge and cause progressive damage to adjacent functioning nephrons
57
Q

What is the epidemiology of polycystic kidney disease?

A

Most commonly inherited kidney disorder, affection 1/800, responsible for nearly 10% of end-stage renal failure in adults

58
Q

What are the presenting symptoms of polycystic kidney disease?

A
  • Usually present at 39-40 years. 20% have no FHx.
  • May be asymptomatic
  • Pain in flanks as a result of cyst enlargement/bleeding, stone, blood clot migration, infection
  • Haematuria (may be gross)
  • Hypertension
  • Associated with intracranial ‘berry’ aneurysms and may present with subarachnoid haemorrhage (sudden onset headache)
59
Q

What are the signs of polycystic kidney disease on examination?

A
  • Abdominal distension, enlarged cystic kidneys and liver palpable, hypertension. Signs of chronic renal failure at late stage
  • Signs of associated aortic aneurysm or aortic valve disease
60
Q

What are the investigations for polycystic kidney disease?

A
  • Ultrasound or CT imaging: Multiple cysts observed bilaterally in enlarged kidneys, sensitivity of detection poor for those under 20 yrs
  • Liver cysts may also be seen
61
Q

What is renal artery stenosis?

A

Stenosis of the renal artery

62
Q

What is the aetiology of renal artery stenosis?

A
  • Atherosclerosis (older pt): Widespread aortic disease involving renal artery ostia
  • Fibromuscular dysplasia (younger patient): Fibromuscular dysplasia is of unknown aetiology but may be associated with collagen disorders, neurofibromatosis and Takayasu’s disease. This may be associated with micro-aneurysms in the mid and distal renal arteries (resembling string of beads on angiography)
63
Q

What are the presenting symptoms of renal artery stenosis?

A
  • History of hypertension in under 50 yrs
  • Hypertension refractory to treatment
  • Accelerated hypertension and renal deterioration on starting ACE inhibitor
  • History of flash pulmonary oedema
64
Q

What is the epidemiology of renal artery stenosis?

A
  • Prevalence is unknown but believed to account for 1-5% of all hypertension; fibromuscular dysplasia occurs in mainly women with hypertension at less than 45 yrs
65
Q

What are the signs of renal artery stenosis on examination?

A
  • Hypertension
  • Signs of renal failure in advanced bilateral disease
  • An abdominal bruit may be heard over the stenosed artery
66
Q

What is the pathogenesis of renal artery stenosis?

A

Renal hypoperfusion stimulated the renin-angiotensin system leading to increased circulating angiotensin II and aldosterone, increasing BP, which is turn, with time, causes fibrosis, glomerulosclerosis and renal failure

67
Q

What are the investigations for renal artery stenosis?

A
  • Non invasive: Duplex ultrasound (technically difficult if obese. Ultrasound measurement of kidney size (predicts outcome after revascularisation, kidneys less than 8cm unlikely to improve)
  • CT angiography or MRA: Often used now, risk of contrast nephrotoxicity
  • Digital subtraction angiography: gold standard assessment
  • Renal scintigraphy
68
Q

What is testicular torsion?

A

Urological emergency caused by the twisting of the testicle on the spermatic cord leading to constriction of the vascular supply and time-sensitive ischaemia and/or necrosis of testicular tissue

69
Q

What is the aetiology of testicular torsion?

A
  • Bell clapper deformity of the common anatomical defect association with the development of intra-vaginal testicular torsion
  • Trauma
70
Q

What is the epidemiology of testicular torsion?

A

Affects males of any age but most commonly adolescent boys

71
Q

What are the presenting symptoms testicular torsion?

A
  • Age under 25 yrs
  • Neonate
  • Testicular pain
  • Intermittent or acute on-and-off pain
  • No pain relief upon elevation of scrotum
  • Nausea and vomiting
  • Abdominal pain
72
Q

What are the signs of testicular torsion of examination?

A
  • Bell clapper deformity
  • Scrotal swelling or oedema
  • Scrotal erythema
  • Reactive hydrocele
  • High-riding testicle
  • Horizontal lie
  • Absent cremasteric reflex
73
Q

What are the investigations for testicular torsion?

A
  • Grey scale ultrasound: presence of fluid and whirlpool sign
  • Power Doppler ultrasound: absent or decreased blood flow in affected testicle
  • Colour Doppler ultrasound
74
Q

How is testicular torsion managed?

A
  • Immediate urological consultation for emergency scrotal exploration
  • Supportive care
75
Q

What are the possible complications of testicular torsion?

A
  • Infarction of testicle/permanent testicular damage/loss of testicles
  • Infertility secondary to loss of testicle
  • Psychological implication of losing a testis
  • Cosmetic deformity
  • Recurrent torsion
76
Q

What is the prognosis for testicular torsion?

A
  • Longer it takes for diagnosis and repair, greater likelihood that pt will develop tissue necrosis, decrease tissue viability, decreased spermatogenesis and possible infertility
  • Recurrent torsion may develop in pts with past history of testicular fixation may years later
77
Q

What is a transurethral resection of the prostate?

A

Operation used to treat benign prostatic hyperplasia

  • Performed by visualising prostate through the urethra and removing tissue by electrocautery or sharp dissection
  • Done with spinal or general anaesthetic
78
Q

What are the indications for transurethral resection of the prostate (TURP)?

A
  • Benign prostatic hypertension if not resolved medically
79
Q

What are the possible complications of transurethral resection of the prostate (TURP)?

A
  • Bleeding
  • Clot retention and clot colic
  • Bladder wall injury such as perforation
  • TURP syndrome: Hyponatraemia and water intoxication from the open prostatic sinusoids during the procedure. Can lead to confusion, changes in mental status, nausea, vomiting and even coma
  • Urinary incontinence
  • Retrograde ejaculation
80
Q

What is urinary catheterisation?

A

A latex, polyurethane, or silicone tube is inserted into a patient’s bladder via the urethra

  • Allows patient’s urine to drain freely from the bladder for collection
  • May be used to inject liquids used for treatment or diagnosis of bladder conditions
81
Q

What are the indications for urinary catheterisation?

A
  • Provide relief of discomfort from bladder distension
  • Decompression of bladder
  • Measure residual urine
  • Management of pts with spinal cord injury, neuromuscular degeneration or incompetent bladders
  • Post-surgery and in critically ill pts to monitor urinary output
  • Prolonged and chronic urinary retention
82
Q

What are the possible complications of urinary catheterisation?

A
  • UTI
  • Allergic reaction to material e.g. latex
  • Bladder stones
  • Injury to urethra
  • Kidney damage
  • Infection of urinary tract, kidney or blood (septicaemia)
83
Q

What are urinary tract calculi?

A
  • Stones consist of crystal aggregates
  • Stones form in collecting ducts and may be deposited anywhere from renal pelvis to urethra
  • Opaque and lucent stones
  • Main sites: pelvic ureteric junction, pelvic brim, ureterovesical junction
84
Q

What is the aetiology of urinary tract calculi?

A
  • Idiopathic
  • Season: variations in Ca and oxylate levels mediated via vid D synthesis and sunlight
  • Dehydration
  • UTIs
  • Drugs: diuretics antacids, acetazolamide, steroids, theophylline, aspirin, allopurinol, vit C and D, indinavir
  • Diet: chocolate, tea, rhubarb, strawberries, nuts, spinach
85
Q

What are the risk factors for urinary tract calculi?

A
  • Recurrent UTIs
  • Metabolic abnormalities: hypercalcuria, hypercalcaemia, hyperthyroid, Addison’s, Cushing’s, vit D excess
  • Urinary pH
  • Congenital: horseshoe kidneys, hydronephrosis
  • Family Hx
  • Drugs
  • Foreign bodies: stents: catheters
86
Q

What is the epidemiology of urinary tract calculi?

A
  • Male: female 3:1

- Peak age: 20-40 yrs

87
Q

What are the presenting symptoms of urinary tract calculi?

A
  • Asymptomatic
  • Renal colic: Pain, nausea & vomiting, cannot lie still unlike peritonitis
  • Renal obstruction: felt in loin, between rib 12 and lateral lumbar muscles
  • Obstruction of lower ureter: bladder irritability, pain in scrotum, labia majora pain
  • Obstruction of bladder/urethra: pelvic pain, dysuria, frequency and interrupted flow
88
Q

What are the signs of urinary tract calculi on examination?

A
  • Usually no tenderness on examination

- Renal angle tenderness to percussion if retroperitoneal inflammation

89
Q

What could be the differential diagnosis for urinary tract calculi?

A
  • Peritonitis: but cannot lie still with renal colic

- Obstruction of mid ureter may mimic appendicitis/ diverticulitis

90
Q

What are the investigations for urinary tract calculi?

A
  • Bloods: FBC, U&Es, calcium, phos, albumin, PTH, vit D, urate, bicarb, serum ACE, thyroid function
  • Urine: Dipstick, microscopy, culture, urine pH, 24h collection, random urine, pregnancy test in females of child bearing age
  • KUB: plain radiograph, shows radio-opaque stones, opaque ( calcium oxalate), semi-opaque (cysteine), lucent (urate)
  • IV urogram: IV contrast may show filling defect in urinary outflow
  • High resolution helical CT abdomen: can exclude AA (presents similarly)
  • Renal US: first line is pregnancy, assess hydronephrosis, may miss smaller stones, cannot differentiate between stones
  • Chemical analysis if stone passed
91
Q

How is urinary tract calculi managed?

A
  • Analgesics: multimodal- weak opioid, NSAIDs, regular paracetamol
  • Rehydrate: oral/IV and stones may be passed naturally if under 5mm
  • Antibiotics: cef or gentamicin
  • Treat UTI/exacerbating factors (cefuroximine/gentamicin)
  • Stones more than 5mm in lower ureter should pass with increased fluid intake
92
Q

How should urinary tract calculi more than 5mm with pain not resolving be managed?

A
  • Medical expulsion therapy
  • Ureteric spasm: Ca channel antagonists, alpha antagonists
  • Extracorporeal shockwave lithotripsy
  • Ureteroscopy and basket
  • Cystoscopy
  • Percutaneous nephrlithomoty
93
Q

What are the possible complications of urinary tract calculi?

A
  • Obstruction and hydronephrosis
  • Ureteric stricture
  • Intrarenal/perinephric abscess
  • Xanthogranulomatous pyelonephritis
  • Urine extravasation
  • Infection
  • Renal failure if primary hyperoxaluria
94
Q

What is the prognosis for urinary tract calculi?

A
  • 20% will not pass spontaneously

- 50% recurrence in 5 years

95
Q

What is a urinary tract infection?

A
  • Characterised by presence of more than 100,000 of colony-forming units per mililitre of urine.
  • UTI’s may affect bladder (cystitis), kidney (pyelonephritis) or prostitis (prostatitis)
96
Q

What is the aetiology of urinary tract infections?

A
  • Usually transurethral ascent of normal colonic organisms
  • The most common organisms is E.coli, others include Proteus mirabilis, Klebsiella and Enterococci (more common in hospitals)
97
Q

What is the epidemiology of urinary tract infections?

A

Common in females: 30% of women experience UTI at some point in their lives

  • UTI may be seen in 5% of pregnant women, 2% of non-pregnant, 20% of elderly living at home and 50% of institutionalised elderly
  • UTI rare in children and young men (if present, suspect an underlying cause)
98
Q

What are the presenting symptoms of urinary tract infections?

A
  • May be clinically silent (asymptomatic bacteruria)
  • Cystitis: Frequency, urgency, dysuria, haematuria, suprapubic pain, smelly urine
  • Pyelonephritis (acute): Fever, malaise, rigors, loin/flank pain
  • Prostatitis: Fever, low back/perineal pain, irritative and obstructive symptoms (e.g. hesitancy, urgency, intermittency, poor stream, dribbling)
  • Elderly: Malaise, nocturia, incontinence, confusion
    Up to 30% of women with UTI symptoms may not have bacteruria
99
Q

What are the signs of a urinary tract infection on examination?

A

May be asymptomatic

  • Cystitis: Fever, abdominal/suprapubic/loin tenderness, bladder distension
  • Pyelonephritis: Fever, loin/flank tenderness
  • Prostatitis: Tender, swollen prostate
100
Q

What are the investigations for urinary tract infections?

A

Mid stream urine for

  • Dipstick test: for blood, protein, leucocytes, nitrites (urinary bacteria reduce nitrates to nitrites)
  • Microscopy, culture and sensitivity
  • If there is sterile pyuria (pus cells with no organisms) consider if this may be partially treated UTI, tuberculosis stones, tumour, interstitial nephritis or renal papillary necrosis
  • Imaging: Renal US or IV urogram may be considered in women with frequent UTIs and in children & men
101
Q

How are urinary tract infections managed?

A
  • Cystitis: if symptomatic, consider local microbiological policies, commonly used agents are oral co-trimoxazole, trimethroprim, nitrofurantoin or amoxicillin (in females) and ciprofloxacin (males)
  • Pyelonephritis: IV gentamicin, cefuroxime or ciprofloxaxin
  • Catheterised patients: Obtain a culture and consider changing catheter. Do not treat unless pt symptomatic as catheters invariably become colonised
  • Prophylaxis: High fluid intake. Regular micturation to keep bladder empty. Cranberry based products reduce frequency of recurrence. In some cases, low dose long-term (6-12 months) antibiotics for women with frequent UTIs
  • Surgical: Rarely necessary. may be necessary for relief of any obstruction and removal of renal calculi
102
Q

What are the possibly complications of urinary tract infections?

A
  • Renal papillary necrosis (in those with underlying renal disease e.g. diabetes mellitus or stones)
  • Renal/perinephric abscess (seen on renal ultrasound)
  • Pyonephrosis (pus in palvicalyceal system)
  • Gram-negative septicaemia
103
Q

What is the prognosis for urinary tract infections?

A
  • Mostly resolve with treatment

- Among pregnant women, 20% develop acute pyelonephritis if not treated, however, there is a high relapse rate

104
Q

What is varicocele?

A

Abnormal dilation of the internal spermatic veins and pampiniform plexus that drains the testis

105
Q

What is the aetiology of varicocele?

A
  • Anatomical features, namely increased hydrostatic pressure in the left renal vein and incompetent or congenitally absent valves, typically implicated as primary cause
  • Incompetent valves within the left internal spermatic vein
106
Q

What is the epidemiology of varicocele?

A

10-15% of men and adolescent boys

107
Q

What are the presenting symptoms of varicocele?

A
  • Presence of risk factors (first degree relative esp. brothers, certain somatometric parameters such as tall/low BMI)
  • Age over 12
108
Q

What are the signs of varicocele on examination?

A
  • Painless scrotal mass
  • Left-sided signs/symptoms
  • Small testicle
  • Infertility
109
Q

What are the investigations for varicocele?

A
  • Scrotal US with colour flow Doppler: presence of varicocele
  • Semen analysis: variable, reduced sperm count, impaired sperm motility (less than 50% motile spermatazoa)
  • Serum FSH + GnRH stimulation: variable, FSH may be elevated (suggesting testicular dysfunction)
  • Serum testosterone: may be low
  • DNA fragmentation index (DFI): increased

Year 3 ICSM Sofia (16 decks)

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