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Y5 Urinary System > List I - Core Conditions > Flashcards

List I - Core Conditions Flashcards

1
Q

What are the causes of chronic kidney disease?

A
  • Diabetic neuropathy
  • Glomerulonephritis
  • Hypertension
  • Systemic disease e.g. SLE, vasculitis, amyloid, myeloma
  • Renal artery stenosis
  • Hereditary e.g. PCKD
  • Chronic pyelonephritis
  • Nephrotoxic drugs
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2
Q

How might CKD patients present?

A
  • Incidental finding on blood or urine tests in investigation of other condition/routine test
  • Hypertension
  • Monitoring “at risk” individuals
  • Symptoms usually occur later at advanced stage
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3
Q

How is kidney function assessed?

A
  • Serum urea - increased with reduced renal excretion
  • Breakdown of amino acids (protein catabolism)
  • Disproportionately high serum urea
  • Catabolic state, high protein intake, gastrointestinal bleed, glucocorticoids
  • Dehydration/cardiac failure
  • Disproportionately low serum urea
  • Low protein intake, liver failure
  • Serum creatinine
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4
Q

What is the problem with creatinine?

A
  • Insensitive marker - can have very impaired kidney function with relatively little creatinine increase
  • Related to musculature
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5
Q

How else is kidney function measured?

A
  • eGFR
  • Calculated from blood results and demographic data
  • Has a degree of error relating to muscle mass - especially extremes
  • Racial correction (multiply 1.2 x if Afro Caribbean / Black patient)
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6
Q

What is the classification of eGFR?

A
  • Stage 1 >90 Normal/high
  • Stage 2 60-90 Mild decrease
  • Stage 3a 45-59 Mild/moderate decrease
  • Stage 3b 30-44 Moderate/severe decrease
  • Stage 4 15-29 Severe decrease
  • Stage <15 Kidney failure
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7
Q

What is an important marker of risk of progression of CKD?

A
  • Proteinuria

* Spot urine sample

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8
Q

How is the cause of CKD investigated?

A
  • Clinical history
  • Biochemistry/hameatology
  • Urine - dipstick, microscopy (cells, casts)
  • Immunology screen (e.g. SLE, vasculitis, myeloma)
  • Renal ultrasound - “normal”, obstruction, cystic disease, scarring, renovascular, renal asymmetry, small kidneys
  • Renal biopsy/angiography
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9
Q

What is CKD associated with?

A
  • Accelerated cardiovascular disease and mortality

* Significant life-expectancy reduction

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10
Q

What are the normal functions of the kidneys?

A
  • Excretory function
  • Homeostasis - fluid balance, BP
  • Endocine - bone metabolism, erythropoiesis
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11
Q

What are the metabolic complications of CKD?

A
  • Anaemia - reduced erythropoietin
  • Bone mineral disorder - e.g. low serum Ca, high PO4, high PTH
  • Lack of vitamin D 1-alpha hydroxylation by kidneys
  • Phosphate retention because low GFR
  • Metabolic acidosis (low sodium bicarbonate on venous bloods)
  • Hyperkalaemia
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12
Q

What are the clinical features of CKD?

A
  • Renal - fluid retention, polyuria, nocturia
  • Cardiovascular
  • hypertension, pulmonary, oedema
  • LVH/dysfunction, vascular disease, dyslipidaemia, vascular calcification
  • Gastrointestinal
  • Anorexia, nausea, vomiting, malnutrition, peptic ulceration
  • Neurological - peripheral neuropathy, restless legs
  • Dermatological - pigmentation, pruritis
  • Endocrine - erectile dysfunction, oligoammenorrhea, reduced fertility/ability to carry pregnancy
  • Musculoskeletal - bone pain, fractures, arthropathy
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13
Q

When should patients be referred to a specialist for renal function?

A
  • eGFR<30
  • Progression
  • Uncertain cause or suspected systemic disease
  • Hereditary
  • Significant proteinuria
  • Haematuria and proteinuria
  • Complications of CKD
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14
Q

What is the management of CKD?

A
  • Treatment of underlying cause of CRF if possible
  • Lifestyle
  • BP control
  • CVS risk reduction
  • Diet
  • Anaemia - erythropoietin
  • Bone disease
  • Vitamin D analogues, phosphate control (diet phosphate binders)
  • Bicarbonate supplements for acidosis
  • Restless legs - sleep hygiene and off licence gabapentin/pregabalin
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15
Q

When should CKD be suspected?

A
  • Incidental finding of:
  • Raised serum creatinine and/or serum eGFR of <60mL/min/1.73m2
  • Proteinuria (ACR >3mg/mmol)
  • Persistent haematuria (2/3 dipstick tests show 1+ or more of blood) after exclusion of UTI
  • Urine sediment abnormalities (RBCs, WBCs, granular casts and renal tubular epithelial cells
  • Be aware that CKD can be asymptomatic in the early stages
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16
Q

If CKD is suspected, what should be asked about in the history?

A
  • General symptoms - lethargy, itch, breathlessness, cramps, sleep disturbance, bone pain, loss of appetite, vomiting, weight loss, taste disturbance
  • Urine output - polyuria, oliguria, nocturia, anuria, obstructive uropathy
  • Nephrotoxic drugs
  • Risk factors - previous AKI
  • Comorbidities or complications
  • Polycystic kidney disease
  • Associated features of anxiety or depression
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17
Q

What are the examination signs for progression of CKD?

A
  • Uraemic odour (ammonia smell to breath)
  • Pallor
  • Cachexia and signs of malnutrition
  • Cognitive impairment
  • Dehydration or hypovolaemia
  • Tachypnoea
  • Hypertension
  • Palpable flank masses with possible hepatomegaly
  • Palpable distended bladder (suggests obstructive uropathy)
  • Peripheral oedema
  • Peripheral neuropathy
  • Frothy urine
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18
Q

What are the initial investigations for CKD?

A
  • Arrange blood tests for serum creatinine and eGFR
  • Advise the person not to eat red meat for 12 hours before the test
  • Arrange early morning urine sample to measure the urine albumin:creatinine ratio(ACR)
  • Arrange a urine dipstick to check for haematuria
  • Check the persons nutritional status, BMI, BP and serum HbA1c and lipid profile
  • Consider arranging a renal tract USS (if indicated)
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19
Q

What is the management of the eGFR result for CKD?

A
  • If eGFR <60mL/min/1.73m2 - repeat the test within 2 weeks
  • If eGFR remains <60mL/min/1.73m2 on repeat, repeat the test in 3 months
  • NB interpret with caution for extremes of muscle mass, pregnancy, has oedema, malnourished or uses protein supplements, or is Asian or Chinese in origin
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20
Q

What is the management of the ACR result for CKD?

A
  • <3mg/mmol (no proteinuria) no action required
  • Between 3 and 70mg/mmol, repeat the test within 3 months
  • 70mg/mmol or more, a repeat test is not needed as this indicates significant proteinuria
  • NB transient increases in urine ACR may be seen with menstruation, UTI, strenuous exercise and upright posture
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21
Q

What is the management of the urine dipstick to check for haematuria in suspected CKD?

A
  • If 1+ or more of blood on dipstick, arrange a mid-stream (MSU) to exclude a UTI and manage accordingly
  • If there is isolated persistent haematuria (2/3 dipstick show 1+ blood or more after exclusion of UTI) with no decrease in eGFR and no proteinuria - see pathway for urological cancer recognition and referral
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22
Q

If the eGFR and the ACR tests are repeated within 3 months, how should the be interpreted?

A
  • Make a diagnosis of CKD if there is persistent reduction in eGFR <60mL/min/1/73m2 and/or proteinuria (ACR >3mg/mmol) lasting for atleast 3 months
  • CKD diagnosis can be excluded if eGFR is persistently >60 and/or ACR is persistently <3mg/mmol and there are no other markers of kidney damage
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23
Q

What how is CKD categorised once a diagnosis is made?

A
  • Using eGFR and urinary ACR
  • Increased ACR is associated with increased risk of adverse outcomes
  • Decreased GFR is associated with increased risk of adverse outcomes
  • Combination multiplies the risk of adverse outcomes
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24
Q

How is ACR combined with eGFR to classify CKD?

A
  • ACR 1/2/3
  • eGFR G1/G2/G3a/G3b/G4/G5
    E.G. G2A2 or G4A3
  • A1=<3mg/mmol normal to mild increase
  • A2=3-30mg/mmol moderately increased
  • A3=>30 Severely increased

See earlier slide or NICE table for details combined with eGFR

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25
Q

Which further measure of renal function which is less influenced by muscle mass, can be used in people with borderline renal function (eGFR values between 45-59 with no evidence of proteinuria) and may be more accurate at determining CKD?

A
  • Cystatin C
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26
Q

How is accelerated progression of CKD defined?

A
  • Persistent decrease in eGFR of 25% or more and a change in CKD category within 12 months; Or
  • Persistent decrease in eGFR of 15mL/min/1.73m2 within 12 months
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27
Q

How is CKD monitored after a confirmed diagnosis?

A
  • Monitor renal function by checking serum creatinine and eGFR together with ACR
  • Repeat the eGFR 3 times over 3 months to monitor progression/identify accelerated
  • If the person is at risk of AKI consider stopping potentially nephrotoxic drugs
  • Arrange FBC to exclude renal anaemia for people with CKD 3b, 4, and 5
  • Arrange serum calcium, phosphate, vitamin D and PTH for people with CKD stage 4 and 5
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28
Q

When should patients be referred?

A
  • 2 week wait referral - Persistent haematuria and urological cancer suspected
  • Referral to a nephrology specialist if:
  • eGFR <30mL/min/1.73m2
  • Accelerated progression of CKD
  • Uncontrolled hypertension
  • Polycystic kidney disease
  • Renal artery stenosis
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29
Q

How should a person with CKD be managed in primary care?

A
  • Assess for and manage risk factors and co-morbidities including:
  • Nephrotoxic drugs
  • Disease progression
  • Lifestyle risk factors
  • Associated anxiety or depression
  • Risk of CV disease
  • Assess for hypertension, if a person is not diabetic and has:
  • ACR <30mg/mmol and associated hypertension, arrange appropriate management
  • ACR >30mg/mmol and associated hypertension, prescribe a low cost renin-angiotensin antagonist (lisinopril or losartan) do not prescribe a combination
  • ACR <70mg/mmol, aim for a BP target of systolic <140mmHg (target 120-139mmHg) and diastolic <90mmHg
  • ACR >70mg/mmol, aim for a BP target of systolic <130mmHg (target 120-129mmHg) and diastolic <80mmHg (same for ACR >3 with DBM)
  • Uncontrolled despite 4 antihypertensive drugs, arrange referral
  • If a person has ACR of 70mg/mmol or more (irrespective of BP or CV disease - prescribe a lisinopril or losartan to achieve the optimal tolerated dose and arrange referral to a nephrologist
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30
Q

What should the BP target range be for a person with diabetes and CKD?

A
  • Systollic <130mmHg (target range 120-129) and diastolic <80mmHg
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31
Q

What should all people with CKD be prescribed?

A
  • Lipid lowering therapy with a statin
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32
Q

What should all people with CKD be prescribed for the secondary prevention of CVD?

A
  • Antiplatelet treatment - low dose aspirin
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33
Q

Which immunizations should be offered to people with CKD?

A
  • Influenza

* Pneumococcal

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34
Q

What self management advice should be given to people with CKD?

A
  • Provide information - www.kidneycare.org
  • Advise on lifestyle measures - stop smoking, drink alcohol in moderation, maintain a healthy body weight, eat a healthy diet and take regular exercise
  • For end stage disease specialist dietary advice about potassium, phosphate, calorie and salt intake may be arranged by the specialist
  • Advise the person to avoid over thecounter NSAIDs, avoid herbal remedies and protein supplements with caution
  • Advise on the increased risk of AKI with intercurrent illness
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35
Q

How would you explain CKD to a patient?

A
  • Chronic kidney disease is a progressive long term condition where the kidneys dont work as well as they used to
  • This can result in tiredness, swelling, breathlessness, feeling sick and even blood in the urine
  • There are many different possible causes which can include high BP, diabetes, older age, infections, polycystic kidney disease, medications such as NSAIDs
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36
Q

What are the indications for renal replacement therapy?

A
  • Uraemic sypmtoms
  • Fluid overload
  • eGFR 5-7 if no symptoms
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37
Q

What is the problem with mineral bone disease in CKD?

A
  • 1-alpha hydroxylation normally occurs in the kidneys - CKD leads to low vitamin D
  • Kidneys normally excrete phosphate - CKD leads to high phosphate

Result of this is:

  • High phosphate level drags calcium from the bones, resulting in osteomalacia
  • Low calcium - due to lack of vitamin D, high phosphate
  • Secondary hyperparathyroidism - due to low calcium, high phosphate and low vitamin D
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38
Q

What is the management of mineral bone disease in CKD (high phosphate, low vitamin D and low calcium) seconday hyperparathyroidism?

A
  • Aim is to reduce phosphate and parathyroid hormone levels
  • Reduced dietary intake of phosphate is the first line management
  • Phosphate binders
  • Vitamin D - alfacalcidol, calcitriol
  • Parathyroidectomy may be needed in some cases
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39
Q

What are phosphate binders?

A
  • Aluminium based binders are less commonly used now
  • Calcium based binders
  • Problems include hypercalcaemia and vascular calcification
  • Sevelamer
  • A non-calcium based binder that is now increasingly used
  • Binds dietary phosphate and prevents its absorption
  • Also appears to have other beneficial effects including reducing uric acid levels and improving the lipid profiles of patients with chronic kidney disease
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40
Q

How is hypertension managed in patients with CKD?

A
  • Majority of patients with CKD will require more than two drugs to treat hypertension
  • First line is ACEi - particularly useful in proteinuric renal disease (e.g. diabetic nephropathy) - these drugs tend to reduce filtration pressure - small fall in eGFR and rise in creatinine can be expected
  • NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, any rise should prompt further monitoring and exclusion of other causes e.g. NSAID’s
  • Furosemide is useful as a anti-hypertensive in patients with CKD, particularly when the GFR falls below 45 ml/min - it has the added benefit of lowering serum potassium - high doses are usually required
  • If the patient becomes at risk of dehydration e.g. gastroenteritis then consideration should be given to temporarily stopping the drug
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41
Q

How should hyperlipidaemia be managed in people with CKD?

A
  • Atorvastatin 20mg should be offered to patients with CKD
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42
Q

What is acute kidney injury?

A
  • Characterised by a decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte and acid base homeostasis
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43
Q

How are the causes of AKI categorised?

A
  • Pre-renal (most common) - due to reduced perfusion to the kidneys leading to a decreased GFR, usually reversible with appropriate early treatment
  • Intrinsic renal - consequence of structural damage to the kidney for example tubules, glomeruli, interstitium, and intrarenal blood vessels
  • Post renal (least common 10%) - due to acute obstruction of the outflow of urine resulting in increased intratubular pressure and decreased GFR
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44
Q

What are the causes of pre-renal AKI?

A
  • Hypovolaemia - dehydration, haemorrhage, gastrointestinal losses, renal losses, burns
  • Reduced cardiac output - heart failure, liver failure, sepsis, drugs
  • Drugs that reduce blood pressure, circulating volume or renal blood flow - ACEi, ARB’s, NSAIDs, loop diuretics
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45
Q

What are the post renal causes of AKI?

A
  • Obstruction - renal stones, blocked catheter, enlarged prostate, genitourinary tract tumours/masses, neurogenic bladder
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46
Q

What are the risk factors for AKI?

A
  • Age 65 or older
  • History of AKI
  • CKD eGFR <60
  • Symptoms or history of obstruction or conditions leading to urological obstruction
  • Chronic conditions such as heart failure, liver disease and diabetes mellitus
  • Neurological or cognitive impairment or disability
  • Sepsis
  • Oliguria (urine output <0.5mL/kg/hr)
  • Nephrotic drugs within the last week (especially if hypovolaemic) e.g. NSAIDS, ACEi, ARB’s and diuretics
  • Exposure to iodinated contrast agents within the past week
  • Cancer and cancer therapy
    Immunocompromise (HIV)
  • Toxins (herbal remedies, poisonous plants and animals)
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47
Q

What are the complications of AKI?

A
  • Hyperkalaemia - usually asymptomatic until severe but can cause muscle weakness, paralysis, cardiac arrhythmias or in extreme cases cardiac arrest
  • Other electrolyte imbalances for example hyperphosphataemia, hyponatraemia, hypermagnesaemia, hypocalcaemia
  • Metabolic acidosis - altered consciousness, circulatory collapse and hyperventilation
  • Volume overload (peripheral and pulmonary oedema - tachpnoea, tachycardia, cyanosis, lung crepitations
  • Uraemia - occurs in severe AKI - confusion, lethargy, altered consciousness
  • CKD and end stage renal disease
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48
Q

What are the signs and symptoms of AKI?

A
  • Nausea and vomiting, or diarrhoea, evidence of dehydration
  • Reduced urine output or changes to urine colour
  • Confusion, fatigue and drowsiness
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49
Q

What is the criteria used to diagnose AKI?

A

Any of the following:
* Rise in serum creatinine of 26 micromol/L or greater within 48 hours
(Be aware in the absence of a baseline creatinine value, a high serum creatinine level may indicate AKI, even if the rise in creatinine over 48 hours is less than 26 micromol/L)
* 50% or greater rise in serum creatinine (more than 1.5 times baseline) known or presumed to have occurred within the past 7 days
* Fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours

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50
Q

How is a person with suspected AKI assessed?

A

Assess volume status by checking:

  • Volume status
  • Fluid intake and losses
  • Peripheral perfusion (CRT)
  • HR/BP (any postural changes)
  • JVP
  • Moistness of mucous membranes, skin turgor
  • Changes in urination pattern
  • Peripheral oedema and pulmonary crackles
  • Renal function and serum potassium level (to exclude hyperkalaemia)
  • For underlying causes
  • Diarrhoea and vomiting
  • Recent symptoms suggesting an underlying obstructive cause (LUTS)
  • Hx CVD
  • Underlying inflammatory process - vasculitic rash, arthralgia, epistaxis or haemoptysis
  • Drug history
  • Possibility of rhabomyolysis - MSK injury, overexertion, crush injury, prolonged immobility
  • For renal disease by performing urine dipstick testing for blood, protein, leucocytes, nitrites and glucose
  • Stage of AKI
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51
Q

What are the criteria of stage 1 AKI?

A
  • Rise of creatinine of 26 micromol or more within 48 hours OR
  • Creatinine rise of 50-99% from baseline within 7 days OR
  • Urine output <0.5mL/kg/hr for more than 6 hours
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52
Q

What are the criteria of stage 2 AKI?

A
  • 100-199% creatinine rise from baseline within 7 days OR

* Urine output <0.5 mL/kg/hr for more than 12 hours

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53
Q

What are the criteria of stage 3 AKI?

A
  • 200% or more rise from baseline within 7 days OR
  • Creatinine rise to 354 micromol/L or more with acute rise of 26 mircromol/L or more within 48 hours or 50% or more rise within 7 days OR
  • Urine output <0.3 mL/kg/hour for 24 hours or anuria for 12 hours
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54
Q

What are the features of AKI on examination?

A
  • Hypovolaemia - assess volume status (CFT, HR, BP, JVP, skin turgor, pulmonary oedema, peripheral oedema, urine output, weight)
  • Palpable bladder
  • Signs of vaculitis (weight loss, fever, rash, uveitis, haemoptysis, joint swelling)
  • Bruits (renal artery stenosis)
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55
Q

What are the investigations for AKI?

A
  • FBC
  • U and E’s
  • Bicarbonate
  • LTF’s
  • Calcium
  • Phosphate
  • Consider blood cultures if sepsis suspected
  • Urine dipstick (presence of blood and protein suggests infection or vaculitis)
  • Chest x-ray (pulmoanry infiltrates could indicate fluid, infection or haemorrhage)
  • Renal tract USS (assess renal anatomy and exclude renal tract obstruction)
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56
Q

What is the management for AKI in hospital?

A
  • STOP AKI
  • Sepsis - complete sepsis 6 if suspected
  • Toxins - stop/avoid nephrotoxins e.g. Gentamicin, NSAID’s, iodinated contrast
  • Optimise blood pressure
  • Volume status assessment, IV fluids, consider holding antihypertensive medications, consider vassopressors
  • Prevent harm - treat complications (e.g. hyperkalaemia, pulmonary oedema, acidosis, pericarditis), identify cause e.g. obstruction, review all medications and doses, refer if renal replacement therapy indicated (e.g. intractible hyperkalaemia, pH <7.15, intractible pulmonary oedema, uraemic pericarditis or encephalopathy), monitor (daily volume assessment, fluid balance, U and E’s, bicarbonate)
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57
Q

What is urea?

A
  • Catabolism of amino acids / protein
  • Increased serum concentration with reduced renal excretion
  • Relatively high serum urea
  • Catabolic state, high protein intake, gastrointestinal bleed, glucocorticoids
  • Dehydration/cardiac failure

Relatively low urea
- Low protein intake, liver failure

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58
Q

What is creatinine?

A
  • Production is related to muscle mass
  • Serum concentrations increased with reduced renal excretion
  • Relatively high serum creatinine
  • Large muscle mass (young, muscular, male)
  • Relatively low serum creatinine
  • Low muscle mass (elderly, wasting, amputees, female)
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59
Q

What is the problem with creatinine in terms of identify kidney disease?

A
  • It is an insensitive marker

* Levels can remain low until eGFR is more significantly reduced

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60
Q

What are the features of proteinuria in relation to CKD?

A
  • Important marker of progression of CKD
  • Traditionally measured by 24 hr urine excretion
  • In practice is quantified by spot urine sample (preferably morning) for protein/creatinine ratio (PCR) in urine, or albumin/creatinine ratio (ACR)
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61
Q

What are the renal effects of CKD?

A
  • Fluid retention
  • Polyuria
  • Nocturia (fluid depletion)
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62
Q

What are the CV effects of CKD?

A
  • Hypertension
  • Pulmonary oedema
  • LVH/dysfunction
  • Vascular disease
  • Dyslipidaemia
  • Vascular calcification
  • Pericarditis
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63
Q

What are the GI effects of CKD?

A
  • Anorexia
  • Nausea
  • Vomiting
  • Malnutrition
  • Peptic ulceration
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64
Q

What are the neurological effects of CKD?

A
  • Peripheral neuropathy
  • Myoclonic jerks
  • Encephalopathy
  • Seizures
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65
Q

What are the dermatological effects of CKD?

A
  • Pigmentation

* Pruritis

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66
Q

What are the endocrine effects of CKD?

A
  • Erectile dysfunction
  • Oligoammenorrhoea
  • Reduced fertility
  • Ability to carry pregnancy
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67
Q

What are the MSK effects of CKD?

A
  • Bone pain
  • Fractures
  • Arthropathy
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68
Q

What are the risk factors for progression of CKD?

A
    • More advanced CKD stage (lower GFR)
    • BP control
    • Proteinuria or albuminuria
  • Race, gender
  • Smoking
  • Hyperglycaemia, hyperlipidaemia
  • Obesity
  • CVS disease
  • Nephrotoxic drugs
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69
Q

What aims of management of hypertension in CKD?

A
  • Hypertension is very common in CKD
  • Major risk factor affecting the rate of progression of chronic renal failure
  • High BP contributes to accelerated CVS disease in CKD
  • In CKD aim for BP down to <140/90
  • If CKD + diabetes or ACR of 70 mg/mmol aim for <130/80
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70
Q

What is the first line anti-hypertensive medication in CKD?

A
  • ACEi/ARB - particularly where albuminuria/proteinuria (except renal artery stenosis)
  • Also indicated for ‘normotensive’ proteinuria
  • May cause transient decrease in GFR
  • Profound drop in renal artery stenosis, dehydration
  • Risk of hyperkalaemia
  • Monitoring U and E’s baseline and at 1 week required
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71
Q

What is the haematological abnormality seen in CKD?

A
  • Normochromic normocytic anaemia (anaemia of chronic disease) - reduced erythropoietin production
  • Bleeding tendency - reduced platelet aggregation
  • Reduced immunity - e.g. reduced response to hepatitis B vaccination
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72
Q

What is this pattern of abnormalities showing?

Serum calcium 2.14 mmol/L (2.2-2.6)

Serum phosphate 1.83 mmol/L (0.8-1.4)

Serum PTH 46 mmol/L (0.9-5.4)

A
  • Secondary hyperparathyroidism and hyperphosphataemia due to CKD
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73
Q

What are the two main factors in the pathophysiology of renal bone disease in CKD?

A
  • Reduced production of 1 alpha hydroxylase (leads to low vitamin D leads to osteomalacia or rickets)
  • Increased levels of phosphate due to reduced clearance

Leads to reduced serum calcium

  • Secondary hyperparathyroidism (high PTH + low Ca)
  • Tertiary hyperparathyroidism (high PTH + high Ca)
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74
Q

What is the treatment of bone disease in CKD?

A
  • Low calcium/high PTH
  • Active vitamin D analogues e.g. alfacalcidol
  • High phosphate
  • Dietary restriction
  • Phosphate binder medication with meals
  • Dialysis
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75
Q

What is the dietary guidance in CKD?

A
  • Varies according to degree of impairment eGFR and individual patient results
  • Salt intake restriction
  • Phosphate, potassium - restrict as needed
  • Calories (avoid/treat obesity and malnutrition)
  • Avoid (or treat) malnutrition
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76
Q

Which drugs should be cautious/contraindicated in patients with CKD?

A
  • Impaired excretion - potential serious toxicity (dose reduction or avoid)
  • Digoxin, aminoglycosides, acyclovir
  • Nephrotoxins / reduce renal function
  • NSAIDs
  • Metabolic effects
  • Hyperkalaemia (ACEi, ARB, amiloride, spironolactone, potassium sparing supplements)
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77
Q

What is the approach to the management of advanced CKD?

A
  • Pre-dialysis counselling/assessment/modality

* Dialysis/transplantation/conservative management

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78
Q

What does dialysis do?

A
  • Replaces excretory role of kidney (much lower clearance) - diffusion solutes between blood and dialysis fluid
  • Removes excess water from the patient
  • Options of haemodialysis and peritoneal dialysis
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79
Q

What is the process of haemodialysis?

A
  • Diffusion of solutes between patients blood and dialysis fluid in artificial kidney
  • Typical patient dialyses for 4 hours 3 times per week
  • Access ideally via AV fistula
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80
Q

What is the process of peritoneal dialysis?

A
  • Diffusion of solutes between the patients blood in peritoneal capillaries and dialysis fluid in peritoneal cavity
  • CAPD (continuous ambulatory peritoneal dialysis) - typically 4 x 2-3 litres exchanges per day
  • APD (automated PD) - several exchanges by machine whilst asleep at night
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81
Q

What is the role of kidney transplantation in CKD?

A
  • Best rehabilitation and patient survival
  • Donor sources
  • Deceased donor (national list)
  • Live donor - related, altruistic
  • Lifelong immunosuppression
  • Transplant failure may occur after time
  • Significant proportion of patients not suitable for transplantation due to other medical conditions
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82
Q

What is the role of medical / palliative treatment in (end stage) CKD?

A
  • Patients may opt to not have life preserving dialysis/transplantation
  • Often elderly/multiple comorbidity - benefits of life may be uncertain vs negative impact on quality of life
  • Facilitated by advanced discussion and planning (when relatively well)
  • Many electively opting for conservative care die of other causes than renal failure
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83
Q

What is microalbuminuria?

A
  • Increased urinary albumin excretion but below level that registers on protein dipstick
  • Normally small amount of protein (small molecules) in urine, but very little albumin (large protein) - increase suggests ‘glomerular leakiness’
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84
Q

Why does microalbuminuria in diabetes matter?

A
  • Risk of progression to established diabetic nephropathy (persistent proteinuria then declining function)
  • CVS risk and increase in diabetes complications
  • Consider treatment options
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85
Q

What is the sequence in progression of albumin excretion rates?

A
  • Normal - 10-30 mg/day
  • Microalbuminuria - 30-300 mg/day
  • Macroalbuminuria - 300+ mg/day
  • Nephrotic syndrome
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86
Q

What is a normal ACR for males and females?

A
  • Males - 2.5 mg/mmol

* Females - 3.5 mg/mmol

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87
Q

What is the hall mark of established nephropathy?

A
  • Persistent dipstick proteinuria
  • Associated with other microvascular complications e.g. retinopathy
  • Typically progressive CKD
  • High CVS risk (DM + CKD)
  • CKD management principles apply - especially RAS blockade i.e. ACEi or ARB
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88
Q

What is the approach to the management of diabetes in CKD?

A
  • Stop metformin when eGFR <30 (risk lactic acidosis)
  • Drug dose alterations for oral drugs
  • Reducing insulin requirements / hypoglycaemia with worsening kidney function
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89
Q

What are the 3 main types of urinary incontinence?

A
  • Stress
  • Urge
  • Mixed
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90
Q

What are the specific symptoms to ask about for urinary incontinence?

A
  • Frequency
  • Nocturia
  • Dysuria
  • Haematuria
  • Urgency
  • Urge incontinence
  • Stress incontinence
  • Difficulty initiating urination
  • Incomplete emptying
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91
Q

What is the management advice for stress incontinence?

A
  • Lifestyle changes - reduce/stop caffeine, smoking and fizzy drinks, lose weight
  • Physiotherapy - pelvic floor exercises at least 8 contractions 3 times per day for 3 months
  • Follow up in 3 months
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92
Q

What is the management advice for urge incontinence?

A
  • Lifestyle changes - reduce/stop caffeine, smoking and fizzy drinks, lose weight
  • Physiotherapy - pelvic floor exercises at least 8 contractions 3 times per day for 3 months
  • Bladder diary (3 days minimum) bladder drills
  • +/- Anticholinergic +/- Vaginal Oestrogens
  • Follow up in 3 months
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93
Q

What can be used to distinguish between urge and stress urinary incontinence?

A
  • Urodynamics
  • Stress - no rise in Pdet
  • Urge - no rise in Pabd
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94
Q

What is the drug used to manage urinary stress incontinence (after failure of pelvic floor exercises)?

A
  • Duloxetine
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95
Q

What are the further management options for urinary urge incontinence?

A
  • Second anticholinergic
  • Cystoscopy and botox - percutaneous posterior nerve stimulation
  • Percutaneous sacral nerve stimulation
  • Augmentation cystoplast or urinary diversion
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96
Q

How do patients report a pelvic organ prolapse?

A
  • Feel like something is coming down - worse on lifting/walking/end of day
  • Usually not painful just uncomfortable
  • Lower back pain
  • Discomfort during intercourse
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97
Q

Which parts of the pelvic organs prolapse?

A
  • Anterior vaginal wall
  • Lower 1/3 cystocele
  • Upper 2/3 urethrocele
  • Posterior vaginal wall
  • First 1/3 deficient perineum
  • Middle 1/3 rectocele
  • Upper 1/3 enterocele
  • Cervix and uterus
  • Vault (if had a hysterectomy)
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98
Q

How is pelvic prolapse graded?

A
  • 0 = Normal position for each respective site
  • 1 = Descent half way to the hymen
  • 2 = Descent to the hymen
  • 3 = Descent halfway past the hymen
  • 4 = Maximum possible descent (Procidentia)
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99
Q

What is the treatment for prolapse?

A
  • Conservative management - weight loss, avoid heavy lifting, pelvic floor exercises
  • +/- Pessary - change every 6 months
  • Surgery
  • Anterior/posterior repair
  • Vaginal hysterectomy
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100
Q

What is mesh treatment?

A
  • TVT for incontinence - Tension free vaginal tapes (for stress incontinence) are mesh and have been used for over 20 years - small piece of mesh sits under the urethra
  • Mesh for prolapse - previously used for prolapse repair- large amounts of mesh were inserted behind the vaginal walls
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101
Q

What is the problem with mesh for prolapse?

A
  • Mesh erosion and chronic pain can occur after both procedures
  • Chronic pain and dyspareunia are much more common when mesh is used for prolapse repair
  • Lots of complaints of pain and subsequent litigation cases have lead to mesh for prolapse repair to be taken off the market
  • Tape for stress incontinence continues to be used after carefully counselling patients
102
Q

What is the classification system for uterovaginal prolapse?

A
  • Baden-Walker
103
Q

What is nephrotic syndrome?

A

Triad of:

  • Proteinuria (>3g/24hr) causing
  • Hypoalbuminaemia (<30g/L) and
  • Oedema
104
Q

Which conditions can cause nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephropathy
  • Focal segmental glomerulosclerosis
  • Amyloidosis
  • Diabetic nephropathy
105
Q

How can nephrotic syndrome be further classified?

A
  • Steroid sensitive NS 90%

* Steroid resistant NS 10%

106
Q

How common is NS?

A
  • 1/50,000 most common in 1-6 yrs (MCD)
107
Q

What is the pathophysiology of NS?

A
  • Increased capillary wall permeability at glomerular basement membrane leads to proteinuria
  • Hypoalbuminaemia leads to reduced oncotic pressure and extravasation of fluid (including Na+) into interstitium
  • Reduced Ig leads to increased risk of infection with capsulated bacteria (pneumococcal)
  • Causes a prothrombotic state - increase in hepatic production of clotting factors/fibrinogen while urinary loss of antithrombin III, protein C, protein S
  • Hyperlipidaemia - increased hepatic synthesis of LDL/VLDL cholesterol while urinary loss of HDL cholesterol
  • Histology - minimal change GN has mild changes on renal biopsy (most amenable to therapy)
108
Q

What are the symptoms of NS?

A
  • Acute - children
  • Insidious - adults
  • Hypoalbuminaemia - generalised oedema, most noticeable in the morning, periorbital (early sign), leg/ankle, scrotal/vulval (late sign), increased weight, abdominal distention (ascites), SOB (pleural effusions)
  • Hypovolaemia - feeling faint, anorexia, V/D, oliguria, frothy urine, pain in abdomen, limbs, gut, head,
109
Q

What are the potential complications of NS?

A
  • Recurrent infections (pneumonia/cellulitis)

* DVT/PE

110
Q

What are the signs of NS?

A
  • BP up/down
  • Oedema (periorbital, sacral, scrotal, vulval)
  • Bibasal lung crepitations
  • Renal mass (late)
  • Measure weight (compare with previous values if known)
111
Q

What are the blood investigations of NS?

A
  • FBC - Hb: haemoconcentration in MCD, increased MCV in hypovolaemia
  • U and E’s up/down in MCD
  • LFT’s - albumin <30, raised ESR/CRP, increased cholesterol, increased triglycerides
  • Serology - screen for underlying cause - antistreptolysin O (ASO titre) raised in post strep GN
  • Auto antibodies - ANA, ANCA, anti-dsDNA, anti-GBM, RhF - Igs, HBsAg - membranous GN
  • Complement - C3 reduced in membranoproliferative GN, reduced C3/C4 in post strep GN
112
Q

What are the urine investigations for NS?

A
  • MSU - dipstick - proteinuria (>3+)
  • MCandS - microscopy (granular and hyaline casts, occasional RBC)
  • 24 hr urine sample - > 3.5 g proteinuria/24 hr
  • Urinary Na+ <20 mmol/L
  • Creatinine clearance
  • Increased ACR
113
Q

What imaging can be done for NS?

A
  • Renal USS for both kidneys - +/- biopsy for adults
114
Q

What samples can be taken for NS?

A
  • MC and S - Throat swab - post strep GN
  • Renal biopsy - done in all adults (histological analysis) - not done in children as assumed MCD
  • Trial of oral steroids in children - if non-responsive then consider renal biopsy
115
Q

What is the conservative approach to the management of NS?

A
  • Risk factor modification
  • Stop smoking
  • Exercise
  • Diet (fluid restriction, low salt, more calories)
  • BP - optimise aim for <125/75 with ACEi
  • Lipid lowering therapy - statin
  • Monitoring
  • Regular dipstick
  • U and E
  • BP
  • Fluid balance
  • Daily weights
116
Q

What is the medical approach to the management of NS?

A
  • Treat the underlying cause
  • Treat any infections as appropriate
  • Diuretics
  • Frusemide 80-250mg/24hrs po
  • Aim to reduce weight, 1kg/24 hrs
  • High dose steroids
  • Prednisolone 60mg/24 hr po (reduce dose when responding < 1+ proteinuria/ increased albumin +/- PPI for gastroprotection
  • Albumin transfusion - if abdominal / scrotal pains ?
  • Thromboprophylaxis - if immobile / albumin <20 LMWH
  • Immunosuppression
  • ACEi - slow the progression of renal impairment in chronic nephrotic syndrome
117
Q

What are the potential complications of NS?

A
  • Hypovolaemia - acute renal failure
  • Infection - pneumonia/cellulitis
  • Thrombosis - 40% renal vein, DVT, arterial
  • Protein calorie malnutrition
  • Hypercholesterolaemia
118
Q

What is the mortality of NS?

A
  • 1-2% due to infections, thrombosis
119
Q

What is the approach to the prevention of NS?

A
  • Secondary prevention - pneumococcal vaccination (all patients), prophylactic penicillin (children with relapsing type)
  • Hyperlipidaemia - statins (all patients while they have features of nephrotic syndrome)
120
Q

What is bladder cancer?

A
  • Type of transitional cell carcinoma which can affect anywhere from the renal pelvis, ureter, (bladder), or urethra
121
Q

What are the risk factors for bladder cancer?

A
  • Age >40 yrs
  • Smoking
  • Occupation - b-naphthylamine: once absorbed it is metabolised in liver and activated in urine - chemical/rubber/aniline dye manufacture
  • Drugs - cyclophosphamide
  • Chronic bladder irritation - infection, prolonged catheterisation, calculi
  • Schistosomiasis - N. America - causes SCC
122
Q

How common is bladder cancer?

A
  • 20/100000/yr in UK
  • M:F = 4:1
  • Increased in caucasians, peak 60-70y (increased with advancing age)
123
Q

What is the pathological process of bladder cancer?

A
  • Exposure - latent period (25 yrs) - development of cancer
  • Histological types
  • Urothelial/transitional cell carcinoma (TCC most common)
  • SCC 5%
  • Primary adenocarcinoma 1-2%
  • Carcinoma in situ (urothelium)
  • Subtypes
  • Graded G1-3 based on degree of differentiation
  • Superficial papillary tumours 75% G1
  • Infiltrative G2
  • Invasive - less common G3
124
Q

What is the spread of bladder cancer?

A
  • Local - tumour grows, outgrows blood supply, bleeding/haematuria, irritates the bladder, filling symptoms, local invasion, may cause pain, infiltrates ureters, obstructive renal impairment, invades urethral orifice, bladder outflow obstruction
  • Metastatic - liver, lungs
  • Paraneoplastic - uncommon (persistent pyrexia)
125
Q

What are the presenting clinical features of bladder cancer?

A
  • Intermittent painless, frank haematuria (85%) or incidential microscopic haematuria (dipstick)
  • Bladder irritation - frequency, urgency, nocturia, dysuria, pain
126
Q

What are the differential diagnoses for bladder cancer?

A
  • Any haematuria must be investigated as follows:
  • Clinical assessment
  • Abdominal x-ray KUB
  • Renal USS
  • Flexible cystoscopy
127
Q

What are the initial investigations in blood for suspected bladder cancer?

A
  • FBC - WCC raised 33% if UTI present

* U and E’s - raised creatinine due to renal impairment from post renal obstructive cause

128
Q

What are the urine investigations for suspected bladder cancer?

A
  • MSU - dipstick (blood++)

* MC and S and cytology

129
Q

What are the radiological investigations for suspected bladder cancer?

A
  • Abdominal x-ray KUB - exclude renal calculi

* Renal USS - exclude solid renal tumours

130
Q

What further investigations can be done for suspected bladder cancer?

A
  • Flexible cystoscopy - using LA instiller gel as a day case for visual confirmation of bladder cancer
131
Q

What are the management options for bladder cancer?

A
  • Surgical transurethral resection of bladder tumour (TURT)
  • Indications - initial management for all types confirming diagnosis and treatment
  • Procedure - GA/LA - biopsy for histology
  • Problems - bleeding, bladder perforation
  • Endoscopic resection with adjuvant intravesical therapy
  • Indications - superficial bladder cancer (Ta, T1 - but not high grade G3, T1)
  • Procedure - endoscopic resection
  • Problems - systemic absorption of BCG (TB risk)
  • Radical cystectomy and urinary diversion therapy with systemic therapy
  • Indications - detrusor muscle invasive (pT2) bladder cancer (including high grade G3 pT1)
  • Procedure - excision of all bladder (partial in some settings), all anterior pelvic organs (including hysterectomy), regional nodes
  • Urinary diversion (either)
    1) Ileal conduit - section of ileum removed with mesentery, one end turned inside out to be exposed through abdomen, other end connected to ureters
    2) Continent reservoir (requires frequent catheterisation)
    3) Orthotopic - section of ileum removed with mesentery and opened out and upturned onto incised bladder
  • Systemic therapy post cystectomy
  • Chemotherapy - neoadjuvant - increases 5 yr survival chance by 5% or adjuvant
  • Radiotherapy - potential cure for TCC but adenocarcinoma/SCC are radioresistant, can be used alone (but 60% recurrence) or after cystectomy (better 5 yr survival rates)
132
Q

What are the complications / outcomes of bladder cancer?

A
  • 5 year survival rates - treated bladder cancer is 95%
  • Treated but organ confined muscle invasion 50%
  • Treated but extra-vesicle muscle invasion 20%
  • Radical cystectomy 90% 10 yr recurrence free survival
133
Q

What are the secondary / ongoing preventative measures for bladder cancer?

A
  • Regular flexible cystoscopy post surgery if recurrences for:
    1) Superficial bladder cancer post resection - repeat ablation / resection (cystectomy if frequent recurrences)
    2) Invasive bladder cancer - salvage cystectomy + chemotherapy
134
Q

What are the types of prostate cancer?

A
  • Primary - usually adenocarcinoma

* Secondary - usually from TCC from bladder invasion, rarely lymphoma, melanoma

135
Q

What is the role of PSA testing in prostate cancer?

A
  • Early detection - before symptoms develop

* Early treatment - detecting early may help to extend life or facilitate a complete cure

136
Q

What are the signs and symptoms of prostate cancer?

A
  • Localised prostate cancer is often asymptomatic and localised advanced prostate cancer is also frequently asymptomatic
  • Metastases may cause the first symptoms to bones causing pain
  • Suspect prostate cancer in men who have:
  • Any of the following symptoms that are unexplained
  • Lower back, or bone pain
  • Lethargy
  • Erectile dysfunction
  • Haematuria
  • Anorexia/weight loss
  • Lower urinary tract symptoms such as frequency, urgency, hesitancy, terminal dribbling, and/or overactive bladder
  • A prostate that is hard and nodular on DRE - normal DRE does not exclude prostate cancer
  • PSA levels that are raised or rising (urinary tract infection or other possible causes have been excluded)
137
Q

What is prostate specific antigen?

A
  • PSA is a protein produced in normal and cancerous prostate cells
  • PSA is secreted by prostate epithelial cells into prostatic fluid where its function is to liquefy semen and thus allow spermatozoa to move more freely
  • Although PSA is secreted into prostatic fluid and semen, small amounts of PSA are present in the blood
138
Q

What PSA testing?

A
  • Result of altered prostate architecture in prostate cancer, more PSA leaks out increasing the levels in the blood
  • However, PSA is only good to rule out cancer as PSA can be high for other reasons such as benign prostatic enlargement, prostatis and UTI
139
Q

When should PSA testing be offered?

A

Before offering PSA ensure that the man has carefully considered the benefits and risks of PSA tests

  • Offer PSA testing to:
  • Men older than 50 years of age who request a PSA test
  • Consider a PSA test in men with:
  • LUTS - nocturia, urinary frequency, hesitancy, urgency or retention
  • Erectile dysfunction
  • Visible haematuria
  • Unexplained symptoms that could be due to advanced prostate cancer (lower back pain, bone pain, weight loss)
  • Routine screening for prostate cancer is not national policy because the benefits have not been shown to outweigh the risks
  • PSA testing should not be offered to asymptomatic men
140
Q

What are the benefits of PSA testing?

A
  • Early detection - before symptoms develop

* Early treatment - detecting early may help to extend life or facilitate a complete cure

141
Q

What are the limitations of PSA testing?

A
  • False negative PSA tests - about 15% with a negative test may have prostate cancer - 2% with a high grade cancer
  • False positive PSA tests - about 75% of men with a positive PSA test have a negative prostate biopsy
  • Unnecessary investigation - false positive PSA test my lead to invasive investigations such as prostate biopsy and there may be adverse effects (bleeding or infection)
  • Unnecessary treatment - a positive PSA test may result in identification and treatment of prostate cancers which would not have become clinically evident during the man’s lifetime. Adverse effects of treatment are common and serious including urinary incontinence and sexual dysfunction
142
Q

What should men considering a PSA test be advised to use or refer to when making the decision?

A
  • Decision aids:
  • Public Health England - information sheet
  • Online NHS Right Care decision aid
  • SWOP - online decision aid from the Department of Urology of the Erasmus MC
143
Q

What are the clinical criteria for PSA testing?

A

Men should not have PSA testing if they have any of the following:

  • Active urine infection (PSA may be raised for many months)
  • Had a prostate biopsy in the previous 6 weeks
  • Exercised vigorously in the last 48 hours
  • Ejaculated in the last 48 hours

Specimen must reach the laboratory within 48 hours

144
Q

How should the results of the PSA be interpreted?

A
  • Normal PSA level ranges from 0-4 nanograms/mL
  • Upper level of normal may vary according to age and race, PSA test is not diagnostic
  • Men with an elevated PSA may need further investigation, for example biopsy
  • If PSA level in men (of any race) aged 50-69 years is:
  • 3.0 nanogram/mL or higher - refer men urgently using a suspected cancer pathway referral (for an appointment within 2 weeks) to a specialist
  • Within the normal range - low risk of prostate cancer
  • Refer only if there are concerns, for example factors that increase the risk of prostate cancer or an abnormal DRE
  • Use clinical judgement to manage symptomatic men and those aged under 50 who are considered to have a higher risk for prostate cancer
145
Q

When should DRE be offered to assess the risk of prostate cancer?

A

Consider DRE to assess for prostate cancer in men with:

  • Any lower urinary tract symptoms (nocturia, urinary frequency, hesitancy, urgency or retention)
  • Erectile dysfunction
  • Visible haematuria
  • Unexplained symptoms (lower back pain, bone pain, weight loss)
  • Concern about possibility of prostate cancer for example raised PSA
146
Q

What is the referral criteria for prostate cancer?

A
  • Refer the man urgently using a suspected cancer pathway referral (for an appointment in 2 weeks) if:
  • DRE reveals a hard, nodular prostate (suggestive of cancer) or
  • PSA levels are above the age specific reference range. For men 50-69 it is >3.0 nanogram/mL or higher
147
Q

Which investigations are performed in secondary care to confirm or exclude the diagnosis and image to assess the stage of the prostate cancer?

A
  • Transrectal ultrasound (TRUS) - may be used to examine the prostate and determine its size - not reliable enough to exclude prostate cancer
  • TRUS prostate biopsy
  • 10-12 cores of prostatic tissue through the rectum guided by USS
  • Additional biopsies may be taken if a lesion is found on USS
  • If a tumour is detected, histology reveals how well it is differentiated and this is graded by the Gleason score
  • Multiparametric MRI and radioisotope bone scans can be used to assess the prostate gland and determine the extent of locally invasive cancer or presence of distant metastases
148
Q

How is prostate cancer managed in primary care?

A
  • Follow up and monitoring, as well as early recognition and initial management of the complications of the condition and adverse effects of its treatment can be carried out in primary care under shared care arrangements
149
Q

What are the complications of prostate cancer?

A
  • Local invasion - spread to the seminal vesicles, base of the bladder, urethral sphincter or side wall of the pelvis
  • Distant metastases - most commonly spreads to the bones, this can cause pain, pathological fractures or spinal cord compression
  • Lower urinary tract symptoms (LUTS) - early prostate cancer does not usually cause LUTS
  • LUTS may be an indication of advanced incurable prostate cancer
150
Q

What are the risk factors for developing prostate cancer?

A
  • Increasing age - mainly affects men over the age of 50 years
  • Black ethnicity - highest risk life time risk is 1 in 4 for black men, 1 in 8 for white men, black men are also twice as likely to die from the disease
  • Family history of prostate cancer and genetics
  • Weight - obesity and being overweight are associated with advanced
151
Q

How is management of prostate cancer determined in secondary care?

A

It is determined on the man’s prognostic risk which is determined after taking into account:

  • Clinical staging
  • PSA results
  • Gleason score
  • Age, comorbidities and the man’s preferences
152
Q

What are the treatment options for prostate cancer?

A
  • Watchful waiting or active surveillance
  • Radical prostatectomy, external beam radiotherapy or brachytherapy
  • High intensity focused ultrasound or cryotherapy (only in controlled clinical trials)
  • Adjunctive and palliative treatments such as hormone therapy, strontium 9 therapy, radium-223 therapy, chemotherapy or bisphosphonates
153
Q

What does watchful waiting consist of for a patient with prostate cancer?

A
  • Regular follow up in primary care - monitored for disease progression in order to avoid treatment unless symptoms appear
  • Includes regular clinical assessments and repeat PSA testing, but not repeated DRE or prostate biopsies
  • Suitable approach for older men or men with significant comorbidities, or with slow growing tumours who are likely to die from other causes
  • If symptoms develop (for example bone pain) or a rapid PSA rise - review by urological cancer service to consider palliative treatment
154
Q

What does active surveillance consist of and when is it appropriate for prostate cancer?

A
  • Involved frequent serial PSA tests, DRE and prostate biopsies
  • Follows a specific protocol:
  • At enrolment - multi-parametric MRI (mpMRI) if not previously performed
  • Year 1
  • Every 3-4 months measure PSA
  • Every 6-12 months DRE
  • At 12 months prostate rebiopsy
  • Years 2-4
  • Every 3-6 months measure PSA
  • Every 6-12 months DRE
  • Year 5 (and every year thereafter)
  • Every 6 months measure PSA
  • Every 12 months DRE
155
Q

Which patients with prostate cancer is active surveillance suitable for?

A
  • Men with low prognostic risk who are suitable for radical treatment in the event of disease progression
  • Is an option for men with intermediate risk who do not wish to have immediate prostatectomy or radical radiotherapy
  • Not recommended for men who are high risk
156
Q

What are the radical treatments for prostate cancer?

A
  • Radical prostatectomy
  • External beam radiotherapy
  • Brachytherapy
157
Q

What is radical prostatectomy, and when is it appropriate treatment for prostate cancer?

A
  • Aim is removal of the entire prostate gland and eradication of the disease
  • Performed by open, laparoscopic or robot assisted surgery
  • It is an appropriate treatment option for:
  • Localised prostate cancer (rarely offered in >70 years)
  • Biochemical relapse after radical radiotherapy
  • Locally advanced prostate cancer - the surgery alone does not normally eradicate - men normally receive radiotherapy or hormone therapy
158
Q

What are the risks associated with radical prostatectomy?

A
  • Urinary incontinence
  • Erectile dysfunction
  • Incomplete resection of the tumour
  • Approximately 20% develop biochemical or clinical recurrence of prostate cancer
159
Q

What is external-beam radiotherapy, and when is it an appropriate treatment for prostate cancer?

A
  • EBRT directs an external source of radiation at the tumour from outside the body
  • Intensity modulated radiotherapy (IMRT) is the best accepted standard
160
Q

When is EBRT an appropriate treatment option for prostate cancer?

A
  • Localised prostate cancer
  • Recommended for those with a realistic chance of gaining long term control of the disease in combination with 6 months of androgen deprivation therapy before, during or after EBRT
  • For high risk androgen deprivation therapy may be continued for up to 3 years
  • EBRT may be combined with high dose HDR brachytherapy for men with intermediate or high risk
  • Biochemical relapse after radical prostatectomy - recommended for men who experience biochemical relapse with increasing PSA levels after radical prostatectomy
  • Locally advanced disease - may be used in combination with HDR brachytherapy
161
Q

What are the adverse effects of EBRT?

A
  • Short term - bowel and bladder problems
  • Long term - erectile dysfunction and urinary problems
  • Small increased risk of colorectal cancer after EBRT
162
Q

What is high intensity focused ultrasound (HIFU) for prostate cancer?

A
  • Uses ultrasound waves to heat the prostate gland and destroy the tissue
163
Q

When is HIFU used to treat prostate cancer?

A
  • HIFU is not recommended except as part of a clinical trial in which it is compared with established interventions
  • In these circumstances HIFU may be an appropriate treatment option for:
  • Localised cancer of the prostate
  • Biochemical relapse after radiotherapy for prostate cancer
  • Locally advanced disease
164
Q

What are the adverse effects of HIFU?

A
  • Erectile dysfunction
  • Urinary incontinence
  • Rectal damage
165
Q

What is cryotherapy for the use of prostate cancer?

A
  • Used to destroy the prostate tissue by freezing
166
Q

When is cryotherapy used to treat prostate cancer?

A
  • Cryotherapy is not recommended except as part of a clinical trial in which it is compared with established interventions
  • In these circumstances cryotherapy may be an appropriate treatment option for:
  • Localised cancer of the prostate
  • Biochemical relapse after radiotherapy for prostate cancer
  • Locally advanced disease
167
Q

What are the adverse effects of cryotherapy for prostate cancer?

A
  • Erectile dysfunction
  • Urinary incontinence
  • Rectal damage
168
Q

What hormonal treatments are used for prostate cancer?

A
  • Androgen withdrawal
  • Bilateral orchidectomy
  • LHRH agonists - goserelin, leuprorelin, triptorelin
  • LHRH antagonists - degarelix
  • Androgen blockade
  • Cyproterone acetate
169
Q

When are hormonal treatments used for prostate cancer?

A
  • Neoadjuvant therapy
  • Concurrent therapy
  • Adjuvant therapy
170
Q

What are the adverse effects of hormonal therapy for prostate cancer?

A
  • Erectile dysfunction
  • Loss of libido
  • Breast swelling
  • Hot flushes
  • Osteoporosis
171
Q

When is hormone therapy an appropriate option for prostate cancer?

A
  • Localised prostate cancer
  • Neoadjuvant 2-3 months before radical radiotherapy, recommended continued for 2-3 years
  • Degarelix LHRH antagonist is licensed for treatment of men with advanced hormone dependent prostate cancer
  • Metastatic prostate cancer
  • Bilateral orchidectomy and continuous LHRH agonist therapy are options
  • Bicalutamide - preferred option for men who hope to retain sexual function are willing to accept the risk of reduced life expectancy and the possibility of gynaecomastia
  • Abiraterone with prednisolone is an option for hormone-relapsed prostate cancer in men who have no, or mild symptoms after androgen deprivation therapy has failed
  • Enzalutamide is an option for treating metastatic hormone-relapsed prostate cancer in people who have no or mild symptoms after androgen deprivation therapy has failed and before chemotherapy is indicated
172
Q

What is strontium-89 therapy and when is it used for prostate cancer?

A
  • Radio-active isotope strontium Sr-89 is an option for men with hormone relapsed prostate cancer and painful bone metastases
  • Strontium-89 is given intravenously and may be used as an adjunctive treatment together with other therapies (e.g. androgen deprivation therapy)
173
Q

What is radium-223 therapy and when is it used for prostate cancer?

A
  • Radium-223 dicholoride is a radiopharmaceutical agent designed to deliver radiation to bone metastases without affecting normal bone marrow
  • Is an option for treating hormone relapsed prostate cancer and symptomatic bone metastases in men who have already had docetaxel
  • Administered by IV injection every 4 weeks for 6 injections
174
Q

What chemotherapy options are available for prostate cancer?

A
  • Docetaxel - in combination with prenisolone for hormone resistant metastatic prostate cancer
  • Cabazitaxel - in combination with prednisolone for treating metastatic hormone-relapsed prostate cancer in people whose disease has progressed during or after docetaxel
  • Corticosteroids - such as dexamethasone is an option as a third line therapy after androgen withdrawal and anti-androgen therapy for men with hormone-refractory prostate cancer
175
Q

When are bisphosphonates used in men with prostate cancer?

A
  • Offer to men taking androgen deprivation therapy who have osteoporosis - do not routinely offer to prevent osteoporosis
  • Consider for pain relief in men with hormone-refractory prostate cancer when other treatments (including analgesics and pallitive radiotherapy) have failed
176
Q

How should follow up for men with prostate cancer be done?

A

Follow up in primary care and for all men review and manage:

  • Complications of the disease including pain, LUTS and symptoms of spinal cord compression
  • Adverse effects from treatment including sexual dysfunction and urinary incontinence
  • Adverse effects of androgen withdrawal treatment including change in body shape and weight gain, tiredness, hot flushes, loss of libido, erectile dysfunction, gynaecomastia and loss of bone density
  • Quality of life
177
Q

For men who are being managed for prostate cancer with radical treatment, what should their follow up be?

A
  • PSA levels should be measured no earlier than 6 weeks after treatment, then at least every 6 months for 2 years and once a year thereafter
  • After at least 2 years follow up can be carried out by telephone or secure electronic communications to men with stable PSA level who have had no significant treatment complications
  • If there is a biochemical relapse (rising PSA level) an estimated of PSA doubling time should be calculated based on 3 measurements over at least 6 months
  • Refer men with evidence of significant disease progression (rapidly rising PSA level or bone pain) to a urological cancer specialist
178
Q

What are the complications/adverse effects of hormonal therapies including orchidectomy in men with prostate cancer?

A
  • Hot flushes
  • Fatigue
  • Osteoporosis
  • Gynaecomastia
179
Q

What is the treatment for hot flushes in men with prostate cancer (from hormonal therapies) ?

A
  • Offer medroxyprogesterone acetate 20 mg per day for 10 weeks
  • Consider cyproterone acetate 50 mg twice a day for 4 weeks 2nd line
180
Q

What is the treatment for fatigue in men with prostate cancer (from hormonal therapies)?

A
  • Offer supervised resistance and aerobic exercise at least twice a week for 12 weeks to reduce fatigue and improve quality of life
181
Q

What is the treatment for osteoporosis in men with prostate cancer (from hormonal therapies)?

A
  • Do not routinely offer bisphosphonates
  • Consider assessing the fracture risk - offer bisphosphonates to men who have osteoporosis
  • Consider denosumab for men who bisphosphonates are contraindicated or not tolerated
182
Q

What is the treatment for gynaecomastia in men with prostate cancer (from hormonal therapies)?

A
  • Start long term bicalutamide monotherapy (longer than 6 months)
  • Offer referral to a specialist for prophylactic radiotherapy to both breast buds for the first month of treatment
  • If unsuccessful consider tamoxifen weekly
183
Q

What is radiation-induced enteropathy in prostate cancer and how should it be managed?

A
  • Symptoms may include diarrhoea, faecal urgency, steatorrhoea or rectal pain
  • Ensure the patient is offered care from a health care specialist with expertise in radiation induced enteropathy
  • Specialist assessment is likely to involve sigmoidoscopy to ascertain the nature of the radiation injury and exclude IBD and bowel cancer
184
Q

How should sexual dysfunction be managed in men with prostate cancer?

A
  • Tell men before starting androgen deprivation therapy that it may cause loss of libido and possible sexual function
  • Advise the loss of fertility associated with therapy and offer sperm storage
  • Ensure men have access to a sexual health specialist
  • Offer a PDE-5 inhibitor such as sildenafil, tadalafil or vardenafil for men who experience loss of erectile function
  • If PDE-5 inhibitors are ineffective or contraindicated offer a choice of:
  • Intraurethral inserts
  • Penile injections
  • Penile prostheses
  • Vacuum devices
185
Q

How should urinary incontinence or retention be managed in men with prostate cancer?

A
  • Warn men undergoing radical treatment of the likely effects on urinary function
  • Offer a urological assessment - if symptomatic before treatment
  • Ensure access to a specialist
  • Management options include - pelvic floor muscle re-education, bladder retraining or medicines
  • Refer men with intractable urinary incontinence to a specialist surgeon for consideration of an artificial urinary sphincter
186
Q

What is hydronephrosis?

A
  • Distention and dilatation of renal pelvis and calyces

* Can affect the kidneys (nephrosis) or ureters

187
Q

What are the causes of intraluminal hydronephrosis?

A
  • Calculi
  • Blood clot
  • Tumour
188
Q

What are the causes of mural hydronephrosis?

A
  • Meatal stenosis
  • Phimosis
  • Urethral strictures
  • Bladder neck hypertrophy
  • BPH
  • Neuromuscular dysfunction
  • Increase sphincter tone
  • Infection
  • Post-op - pain, inflammation, anaesthetic
  • Drugs - anti-cholinergics, alcohol
  • Late cauda equina syndrome - retention/constipation occurs after a period of incontinence of both
  • Schistosomiasis
189
Q

What are the causes of extra-mural hydronephrosis?

A
  • Constipation
  • Abdominal / pelvic mass
  • Retroperitoneal fibrosis
  • Lymphadenopathy
190
Q

Who is more affected by hydronephrosis?

A
  • Elderly
191
Q

What is the pathophysiology of hydronephrosis?

A
  • Urine reflux backs up the ureter
  • Distention of renal pelvis and calyces
  • Distention/dilatation
  • Atrophy of kidney parenchyma
192
Q

What are the presenting clinical features of hydronephrosis?

A
  • Asymptomatic (unilateral)
  • Loin pain
  • Mass
    +/- Acute urinary retention
  • Enlarged kidney mass palpable (sometimes)
193
Q

What are the differentials for hydronephrosis?

A
  • Other obstructive causes
  • Acute urinary obstruction
  • BPH
194
Q

What are the appropriate investigations for hydronephrosis?

A
  • Blood - FBC, U and E’s
  • MSU - dipstick +/- MC and S
  • Imaging - renal USS - can identify hydronephrosis and hydroureter
  • Anterior or retrograde IV ureterograms
195
Q

What are the medical approaches to management of hydronephrosis?

A
  • Medical management of underlying cause - e.g. BPH

* Relieve the obstruction - catherisation

196
Q

What type of cancer is most common in the kidney?

A
  • Renal cell carcinoma 90%
  • AKA Grwitz tumour/hypernephroma
  • Solid malignant tumour of the kidney
197
Q

What are the risk factors for RCC?

A
  • Smoking
  • Obesity
  • Female
  • Heavy metal exposure (cadmium)
  • Acquired cystic disease (not PCKD)
  • Genetic predisposition (3p26 deletion)
  • von Hippel-Lindau disease 35%
  • Hereditary papillary RCC
  • Dialysis 15% cases
198
Q

How common is RCC?

A
  • 3% of adult malignancies
  • 90% of renal cancer
  • Increased in north america/scandinavia
  • M:F = 1.5:1
  • Peaks age 50/60 years
199
Q

What is von Hippel-Lindau disease?

A
  • Autosomal dominant condition (mutated VHL gene) with:
  • Haemngioblastoma/cavernous haemangioma of cerebellum/brainstem/retina
  • Adenomas/cysts of liver /kidney/pancreas/others
  • Phaeochromocytomas
200
Q

What are the sites of RCC?

A
  • Proximal convoluted tubule epithelium (85%)

* Typically unilateral (bilateral 2%)

201
Q

What are the histological subtypes of RCC?

A
  • Clear cell 80%
  • Papillary 14%
  • Sarcomatoid (most aggressive)
  • Chromophobe (4%)
  • Oncocytic 2%
  • Collecting duct <1%
202
Q

What is the local spread of RCC?

A
  • Increase in size
  • Abdominal mass
  • (Pain)
  • Infiltration of blood vessels
  • (Haematuria)
  • Infiltration of inferior vena cava (from R renal vein - IVC obstruction)
  • Infiltration of left renal vein (obstruction to flow of testicular vein - varicocele)
203
Q

What is the metastatic spread of RCC?

A
  • 30% at presentation
  • Lungs, bone, brain
  • Paraneoplastic syndrome
204
Q

What is the paraneoplastic affect of RCC?

A
  • Polycythema (reduced EPO)
  • Increased calcium (increased PTH)
  • Cushing’s syndrome (increased ACTH)
  • Gynaecomastia (increased prolactin)
  • Increased BP (increased renin)
205
Q

What is hepatic necrosis in the context of RCC?

A
  • May occur in the absence of metastases

- Stauffer’s syndrome - improves following a nephrectomy

206
Q

What are the signs and symptoms of RCC?

A
  • Asymptomatic in 50% if localised - incidental finding
  • Classic triad (<10%)
  • Haematuria (50%)
  • Pain (40%)
  • Abdominal mass (30%)
  • Others
  • Increased BP (22%)
  • Paraneoplastic sydrome (10%)
  • Acute varicocele (2%)
  • Fever (PUO)
  • Malaise
  • Anorexia
  • Weight loss
207
Q

What are the differential diagnoses for RCC?

A
  • Renal cyst
  • PCKD
  • Hydronephrosis
  • Neuroblastoma
  • Lymphoma
  • Sarcoma

Other renal cancers

  • TCC - arise in renal pevis
  • Wilm’s tumour (primary renal tumour)
  • Main abdominal malignancy in childhood 1/100,000
  • Primative renal tubules and mesenchymal cells
  • Present with abdominal mass and haematuria
208
Q

What are the initial investigations for suspected RCC?

A
  • Blood
  • FBC - anaemia/polycythemia
  • ESR raised in advanced
  • U and E’s
  • LFT’s - raised ALP if bone mets
209
Q

What are the urine investigations for suspected RCC?

A
  • MSU - dipstick - blood ++

* MC and S - RBC

210
Q

What are the radiological investigations for RCC?

A
  • Abdominal USS - distinguish solid vs cystic lesion (solid more likely to be malignant) and exclude renal vein/IVC involvement
  • IV urogram - with plain AXR KUB control - distorted kidney outline or calyceal pattern
211
Q

What further investigations can be done for RCC?

A
  • Chest x-ray to screen for lung metastases - ‘cannon ball mets’
  • CT chest and abdomen - Bosniak’s classification - to determine if benign/malignant
  • Benign - cystic/non-enhancing/septated/minimal calcification
  • Malignant - solid/enhancing/irregular/highly calcified
  • MRI - superior to CT for assessing renal vein/IVC involvement (if >3cm)
  • Bone scan - pre-op biopsy - NOT PERFORMED - risk of seeding along needle tract
212
Q

What is the TNM staging system used for RCC?

A
  • T - primary tumour
  • Tx - cannot be assessed
  • T0 - no evidence
  • T1 - limited to kidney <7cm
  • T2 - limited to kidney >7cm
  • T3 - confined to Gerota’s fascia - invades adrenal/perinephric tissue, extends into renal vein/IVC
  • T4 - beyond Gerota’s fascia
  • N - regional nodes
  • N1 - 1 node
  • N2 - >1 node
  • M - distant metastases
  • M0 - none
  • M1 - distant mets
213
Q

What is the Robson staging system for RCC?

A
  • I - confined to kidney
  • II - involves perinephric fat but not beyond Gerota’s fascia
  • III - spread to renal veins
  • IV - beyond Gerota’s fascia, invades adjacent/distant organs
214
Q

What is the medical approach to the management of RCC?

A
  • Metastasis - radiotherapy
  • Reduce size
  • Delay local recurrence
  • Palliate bone mets (but no survival benefit)
  • Chemotherapy - RCC is chemo-resistant
  • Can try immunotherapy with IF-alpha, IF-2, 5-FU, lymphocyte activated killer cells
  • Receptor tyrosine kinase inhibitors e.g. sorafenib, sunitinib have been shown to have superior efficacy compared to interferon alpha
215
Q

What is the surgical approach to the management of RCC?

A
  • Nephrectomy
  • Indications - organ confined RCC curative - laparoscopically or open if too large
  • Types: radical (if >7cm remove mass, perinephric fat and Gerota’s fascia) or partial (nephron sparing if <4cm just affecting poles, solitary kidney +/- adrenalectomy - if upper pole/adrenal invasion)
  • Pre-procedure - renal angiography - if partial nephrectomy being considered
  • Procedure - transperitoneal anterior approach (helps to ligate artery and vein if large/hypervascular) transverse abdominal incision with patient supine
216
Q

What are the prognostic factors for outcomes from RCC?

A
  • Factors
  • Size
  • Stage
  • Nuclear grade
  • Cell type
  • Renal vein
  • IVC involvement
  • Renal pelvic invasion
  • Symptomatic
  • Post radical nephrectomy 5 year survival
  • Stage 1 85%, 2 80%, 3 35%, 4 10%
  • Metastases
  • Solitary pulmonary metastases 70% 5 year survival after resection
  • Disseminated 20% 5 year survival
217
Q

What is urethritis?

A
  • Term typically used for men

* Presents with dysuria and/or urethral discharge although it is asymptomatic in up to 30% of men

218
Q

What is non-gonococcal urethritis?

A
  • Now increasingly referred to as non-specific urethritis (NSU)
  • Common causes include:
  • Chlamydia trachomatis
  • Ureaplasma urealyticum
  • Mycoplasma genitalium
219
Q

What investigations are done for NSU?

A
  • Urethral swab - gram stained, looking for the presence of leukocytes and gram negative diplococci
  • Chlamydia is now increasingly diagnosed using urinary nucleic acid amplifications tests (NAAT)
220
Q

What are the potential complications of NSU?

A
  • Epididymitis
  • Subfertility
  • Reactive arthritis
221
Q

What is the management of NSU?

A
  • Either oral doxycycline for 7 days or single dose of oral azithromycin
222
Q

What are renal calculi?

A
  • Crystal aggregates in the kidney
223
Q

What are the different types of renal calculi?

A
  • Ca2+ oxalate 75%, PO4, struvite (Mg2+ NH3-PO4 10-20%)
  • Urate 5%
  • Hydroxyapatite 5%
  • Cysteine 1%
224
Q

What are the causes of renal calculi?

A
  • Ca2+ (metabolic, idiopathic)
  • Struvite (UTI)
  • Urate (hyperuricaemia)
  • Cysteine (renal tubular defect)
225
Q

What are the causes of hypercalciuria/hypercalcaemia?

A
  • Increased PTH
  • Hyperthyroid
  • Addison’s
  • Cushing’s
  • Lithium
  • Increased vitamin D
  • Neoplasia
  • Sarcoidosis
226
Q

What are the causes of hyperuricosuria / raised plasma urate?

A
  • Alone or with gout
227
Q

What are the metabolic causes of hyperoxaluria?

A
  • Primary / secondary
  • Rhubarb/spinach/tea/nuts/strawberries (increased intake)
  • Intestinal reabsorption in Crohn’s
  • Short bowel syndrome
  • Reduced calcium intake as this can lead to increased oxalate excretion into collecting duct
228
Q

What is the possible metabolic cause of cysteinuria?

A
  • Autosomal recessive disorder
229
Q

What is the cause of renal tubular (hyperchloraemic metabolic acidosis)?

A
  • Impaired acid secretion by the kidney (raised anion gap)
230
Q

How does recurrent UTI lead to renal calculi?

A
  • Mainly struvite

- Proteus - causes alkaline urine, Ca2+ precipitation, NH3 salt formation

231
Q

How does urinary tract abnormality cause renal calculi?

A
  • PUJ obstruction
  • Hydronephrosis - renal pelvis calyces
  • Calyceal diverticulum
  • Horse shoe kidney
  • Uterocele
  • Vesico-ureteric reflux
  • Ureteral stricture
  • Medullary sponger kidney

Foreign bodies

  • Stents
  • Catheters
232
Q

What are the risk factors for developing renal calculi?

A
  • Diet - oxalate inducing
  • Summer - increased Ca2+/oxalate by vitamin D via sunlight
  • Occupation - reduced fluids, dehydration
  • Medications
  • Aspirin
  • Corticosteroids
  • Loop diuretics
  • Thiazides
  • Antacids
  • Acetazolamide
  • Theophylline
  • Allopurinol
  • Vitamin C/D
  • Indinavir
  • FH - 3 x increased
233
Q

How common are renal stones?

A
  • 15% are affected at some point (common)
  • Peaks at 20-40 years
  • M:F = 3:1
234
Q

What is the pathology of the development and location of renal calculi?

A
  • Formation in collecting ducts
  • Sites - anywhere from renal pelvis to urethra but usually pelvi-ureteric junction PUJ, pelvic brim, vesico-ureteric junction
235
Q

What are the presenting features of renal calculi?

A
  • Asymptomatic or
  • Colicky abdominal pain (renal angle between rib 12 lateral edge of lumbar muscles)
  • Upper-ureteric obstruction - severe loin to groin pain or genitals/inner thigh, squeezing/spasm pains, N/V, cannot lie still
  • Mid ureteric obstruction - may mimic appendicitis/diverticulitis
  • Lower ureteric obstruction - may have bladder irritation (filling - frequency, urgency, nocturia), pain in scrotum/penile tip or labia majora
  • Bladder/urethral obstruction - pelvic pain, dysuria, incomplete evacuation with desire (strangury)
  • UTI can co-exist
236
Q

What are the appropriate blood investigations for renal calculi?

A
  • Bloods - FBC, U and E’s , Ca2+, phosphate, bicarbonate, urate, glucose
237
Q

What are the appropriate urine investigations for renal calculi?

A
  • MSU - dipstick - RBC +ve in 90%
  • Urine pH
  • MC and S - consider 24 hr urine for Ca2+, oxalate, urate, citrate, Na+, Cr
238
Q

What are the radiological investigations for renal calculi?

A
  • Abdominal x-ray and CT KUB
  • BAUS recommend a non-contrast CT KUB should be performed on all patients within 14 hrs of admission - if patient has fever or the diagnosis is uncertain, an immediate CT KUB should be performed (97% sensitivity)
  • Look along ureters for calcification over transverse processes of vertebral bodies 90% visible
  • IV urogram - with abdominal x-ray KUB control - radio-opaque contrast injected, serial films taken (abnormal if flow stopped at any point, clubbed/blunted calyces from back pressure, bladder filling defect
  • Contraindications
  • Contrast allergy
  • Severe asthma
  • Pregnancy
  • Metformin
  • Acute renal failure
  • Renal USS
  • Exclude hydronephrosis/hydroureter
  • Spiral non-contrast CT - replacing IVU
239
Q

What is the radiological appearance of different renal calculi after AXR/IVU?

A
  • Ca2+ oxalate
  • Spikey (radio-opaque)
  • Ca2+ phosphate
  • Smooth, may be large (radio-opaque)
  • Struvite
  • Large, horny ‘stag horn’ calculi
  • Urate
  • Smooth, brown (radiolucent)
  • Cysteine
  • Yellow, crystalline (semi-radio-opaque)
240
Q

What is the initial approach to the management of ureteric calculi?

A
  • Size <5mm - initial analgesia with diclofenac 75mg IV/IM or 100mg suppository
  • Fluids - oral or IV if not tolerated
  • Anti-biotics if infection likely - cefuroxime 1.5g/8 h IV
  • Size
    <5mm/lower tract - many pass spontaneously
    >5mm/pain unresolving - medical expulsive therapy
  • Nifedipine 10mg/8h po or tamsulosin (a-blocker) 0.4mg/24h po +/- prenisolone (to reduce inflammation)
  • Watch and wait for 30 days, by then most pass spontaneously (most < or = 1st 48 hrs)
241
Q

What are the surgical options for upper urinary tract renal calculi management?

A
  • Extra-corporeal shock wave lithotripsy (ESWL)
  • Percutaneous nephrolithotomy (PCNL)
  • Open surgery (very rare <1%)
242
Q

What is the indication and process of ESWL (lithotripsy)?

A
  • 1st line if >5mm/2cm visible on AXR but can use ESWL stenting if >2.5cm to reduce post procedure complications - can repeat ESWL if initially unsuccessful
  • Done as outpatient
  • Supine, calculi visualised with fluoroscopy/USS - US waves delivered via shock focus and water filled balloon on overlying skin, shatter the calculus
  • Side effects - renal injury, can increase BP, or lead to DBM
  • Contraindications - pregnancy, obesity, uncontrolled coagulopathies, sepsis
  • Complications - infection, bleeding, renal haematoma (25%), adjacent organ damage (pancreas, spleen, liver), arrhythmias
243
Q

What is the indication and process of PCNL?

A
  • 2nd line if unsuccessful with ESWL and/or >2cm, lower calyx, staghorn, multiple, horseshoe kidney (70-100% clearance)
  • GA needed, patient prone, fluoroscopy guided nephrostomy tract created
  • Remove calculus using nephroscope (if >1cm will require in-situ laser/lithotripsy to shatter them first, then nephrostomy tube left in place to drain them
  • Complications - bleeding, adjacent organ damage, local extravasation of irrigation fluid
244
Q

What are the surgical options for mid lower urinary tract renal calculi management?

A
  • ESWL - 1st line

* Ureteroscopy - 2nd line

245
Q

What is the process of ureteroscopy for mid lower urinary tract renal calculi management?

A
  • Outpatient/GA - +/- laser/lithotripsy
  • Calculi/fragments collected in Dormia basket and extra-cated - +/- insert ureteric stent (double J shape with coils at each end to remain in renal pelvis and bladder - can stay in for up to 4 months)
246
Q

What are the surgical options for bladder calculi management?

A
  • Cystoscopy - if <4cm can be fragmented using lithotrite/stone punch - removed using Ellik’s evacuator
  • Suprapubic cystotomy - if >4cm calculus extracted intact - bladder sutured
247
Q

What are the surgical options for urethral calculi (rare)?

A
  • Cystourethroscopically - if they are in the prostatic urethra, they are pushed into bladder and managed as for bladder
248
Q

What are considered urgent cases for calculi?

A
  • Infection + obstruction
  • Urosepsis
  • Intractable pain
  • Impending acute renal failure
  • Obstructed solitary kidney
  • Bilateral obstructing calculi (where delay might cause permanent loss of renal function)
  • Management - percutaneous nephrostomy for obstruction that requires immediate relief
249
Q

What are the complications of renal calculi?

A
  • Hydronephrosis
  • Hydroureter
  • Superadded infection
  • Urosepsis
  • Acute renal failure
250
Q

What is the advice regarding prevention of renal calculi?

A
  • Primary - diet - drink plenty of fluid, maintain normal Ca2+, diets low in calcium will increase oxalate excretion
  • Secondary
  • Ca2+ calculi - thiazide diuretic (to reduce Ca2+ excretion)
  • Oxalate calculi - reduce intake (spinach, nuts), pyridoxine 20-50 mg/8 hr po can be used
  • Struvite - treat infection promptly
  • Urate - allopurinol 100-300 mg/24 h po, urine alkalinisation (K citrate or NaHCO3 urate more soluble at pH >6)
  • Cysteine - vigorous hydration to keep UO >3L/d, urinary alkalinisation (as above), D-penicillamine (chelates cysteine, but must take pyridoxine to prevent vitamin B6 deficiency)

Y5 Urinary System (3 decks)

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