Week 14 - Renal

Question 1

List the functions of the kidneys

Answer 1

• Metabolic waste excretion e.g. urea/creatinine
• Control of solutes and fluid status
  
  • Regulation of total body water
  • Regulation of body electrolytes
• Blood pressure control
• Acid/base
• Drug metabolism/excretion
• Endocrine functions
  
  • Production of renin
  • Production of EPO
• Mineral metabolism
• Glucose metabolism

Question 2

Where are the glomeruli of the kidneys found?

Answer 2

Outer 1-2cm - cortex

Question 3

What is the primary role of the kidneys?

Answer 3

Maintain fluid and electrolyte homeostasis in reponse to blood pressure and hormones

Question 4

How can kidney function be measured?

Answer 4

Measure what is going out in the urine or what is left in the blood

• Metabolic waste excretion - urea, creatinine
• Control of solutes and fluid status - sodium, potassium, fluid
• Endocrine functions - vitamin D, EPO, PTH

Question 5

Describe the role of the glomeruli

Answer 5

Glomerular Filtration Barrier:

• Blood in through afferent arteriole, out through efferent
• Glomeruli filter plasma
  
  • Large molecules/cells/protein are retained in the glomerular tuft - pass out of the efferent arteriole without being filtered due to size and negative charge
  • Small molecules pass through the glomerular basement membrane into Bowman’s space

Question 6

How is glomerular filtration rate controlled?

Answer 6

• Blood flow
  
  • Angiotensin II - efferent arteriole vasoconstriction
  • Myogenic control
  • SNS - direct vasoconstriction
  • Reduced blood volume sensed by baroreceptor –> SNS/renin –> ADH/Ang II –> increased sodium reabsorption ‘distal sensing’
• Intraglomerular pressure
• Transmembrane pressure - filtration barrier
• Oncotic pressure

Question 7

Describe the structure of the glomerular basement membrane

Answer 7

Glomerular BM made up of podocyte foot processes and capillary fenestrated endothelium

Question 8

Describe the movement of fluid through the renal tubules

Answer 8

• Tubules adjust filtrate content, with collecting ducts absorbing water
• 99% filtrate reabsorbed, small amount of secretion by tubules

Question 9

Why are the kidneys so sensitive to hypoxia?

Answer 9

Very perfusion dependent - 20% of blood volume in kidneys at any one time

Question 10

What measures of kidney function can be tested using dipstick urinalysis?

Answer 10

Blood, protein

Question 11

Describe normal and abnormal proteinuria

Answer 11

• Normal - less than 150mg protein/24 hours
  
  • Albumin 15%
  • Other proteins e.g. Tamm Horsfall, Immunoglobulin 85%
    
    • Tamm Horsfall secreted in tubules + minimal amounts of albumin
  • Glomerular filtration barrier prevents proteins being filtered into urine
• Urinalysis detects albumin
  
  • Damage to glomerular filtration barrier - 70% of protein in urine is albumin
  • Should be negative in healthy
• Dependent on concentration of urine

Question 12

How can urinary protein excretion be measured?

Answer 12

• 24 hours urine collection (grams/24 hours)
  
  • Inconvenient, inaccurate
• Protein:creatinine ratio (PCR) on morning spot sample (mg/mmol)
  
  • Urine PCR 100 = 1g per day
• Albumin:creatinine ratio (mg/mmol)

Question 13

Why is quantification of proteinuria important?

Answer 13

Amount of protein lost in urine important for prognosis

• Risk of declining kidney function increased w/ higher levels of proteinuria

Question 14

Describe the types of haematuria

Answer 14

• Can be blood detectable on dipstick (non-visible haematuria)
• Visible haematuria
  
  • Can come from anywhere in the urinary tract (kidneys, stones, infection, malignancy, cysts, inflammation)
  • Unusual to have visible haematuria from glomeruli - usually further down urinary tract

Question 15

What do U&Es measure?

Answer 15

• Sodium
• Potassium
• Chloride
• Urea
• Creatinine
• eGFR
• +/- bicarbonate

Urea, creatinine and eGFR most important for kidney function

Question 16

List the qualities of an ideal substance to measure kidney function

Answer 16

• Freely filtered at glomerulus
• Not secreted
• Not reabsorbed

Question 17

What is creatinine?

Answer 17

Creatine and phosphocreatine breakdown product - muscle breakdown

Question 18

What impacts creatinine concentration?

Answer 18

• Affected slightly by diet - red meat, supplements
• Concentration affected by plasma volume
• Up to 15% secreted by tubule

Question 19

What can impact the concentration of urea?

Answer 19

• Raised by
  
  • Diet - high protein
  • GI bleed
  • Tissue breakdown e.g. corticosteroid
  • Dehydration - passive reabsorption proximal tubule
• Liver failure lowers urea
• Up to 40% reabsorption
• Less reliable marker for kidney function

Question 20

Define renal clearance

Answer 20

• Renal clearance of a substance = volume of plasma which would by cleared of the substance per unit of time
• Usually expressed as ml/min
• Usually described as Glomerular Filtration Rate (GFR)

Question 21

How is eGFR calculated?

Answer 21

MDRD4 (modification of diet in renal disease 4) formula, based on

• Plasma creatinine concentration
• Age (adults only)
• Gender
• Race

Gives value expressed ml/min per 1.73m2 body surface area

Also CKD-EPI equation for patients with higher levels of eGFR

Question 22

Why is eGFR sometimes misleading as a measure of kidney function?

Answer 22

eGFR dependent on muscle mass - more muscle mass higher serum creatinine

• E.g. 20 y/o 90kg healthy male vs 80 y/o 50kg female w/ CKD
  
  • Both have same creatinine - man has much higher muscle mass, woman has low GFR
• Have to lose 50% of GFR before creatinine increases - kidneys able to compensate
• Normal for one patient may not be normal for another

eGFR assumes stable renal function

• Not a valid measurement when kidney function changing rapidly
• Plasma creatinine concentration could be100micromols/l but if the patient has no kidneys or is making no urine the GFR is actually 0
• Important for drug dosing
• eGFR not suitable in AKI

Question 23

When is eGFR useful?

Answer 23

Staging of CKD

Question 24

Describe the staging of CKD

Answer 24

• Stage 1
  
  • eGFR >90
  • With another abnormality, otherwise regard as normal
• Stage 2
  
  • eGFR 60-89
  • With another abnormality, otherwise regard as normal
• Stage 3
  
  • eGFR 30-59
  • Moderate impairment
• Stage 4
  
  • eGFR 15-29
  • Severe impairment
• Stage 5
  
  • eGFR <15
  • Advanced renal failure

Abnormalities e.g. persistent proteinuria/haematuria, microalbuminuria in diabetes, structural kidney disease such as polycystic kidney disease in adults or reflux nephropathy

Question 25

Define glomerulonephritis

Answer 25

Inflammatory diseases involving the glomerulus * Categorised by biopsy findings * Rare in the general population * Variable natural history and presentation * May be primary or secondary * Kidneys vulnerable to insult due to other disease (secondary) * Few specific treatments

Question 26

How many patients w/ glomerulonephritis will require renal replacement therapy?

Answer 26

20% patients w/ glomerulonephritis reach end-stage renal failure (require transplant or life-long dialysis)

Question 27

How should glomerulonephritis be approached?

Answer 27

1. Presentation, history 2. Kidney biopsy findings 3. Likely cause and specific management

Question 28

Which cells are the targets for injury in glomerulonephritis?

Answer 28

* Mesangial - control matrix between capillaries * Endothelial cells of capillaries esp. in systemic disease * Podocytes - outside of glomerular BM, control size/charge selectivity of filtration barrier, damage = lots of protein in urine * Parietal epithelial cell - lines Bowman's capsule

Question 29

Describe the potential pathological mechanisms of glomerulonephritis

Answer 29

* Antibodies, immune complexes, complement * Pre-formed antibodies travel to glomerulus and form complexes, deposited in kidney and cause damage or activate complement * Cell-mediated mechanisms e.g. cytokines, GFs, proteinuria * Metabolic (e.g. diabetes), genetic (e.g. some podocytopathies), vascular causes (e.g. hypertension)

Question 30

List the potential secondary causes of glomerulonephritis

Answer 30

* CV * Subacute bacterial endocarditis * Respiratory * Bronchiectasis * Lung cancer * TB * Pulmonary renal syndromes * Infectious diseases * Hepatitis * HIV * Chronic infections * Antibiotics * Malaria * Rheumatological * RA * Lupus * Amyloid * Connective tissue disease * Drugs * NSAIDs * Bisphosphonates * Heroin * Gastrointestinal * Alcoholic liver disease * IBD * Coeliac disease * Diabetes * Haematological * Myeloma * CLL * Polycythemia rubra vera

Question 31

How should a patient be investigated for glomerulonephritis

Answer 31

* Full medical and drug (including recreational) history * Basics - U&Es, dip urine for blood, quantify proteinuria, check albumin, check USS Glomerulonephritis screen: * ANCA * Anti-GBM * ANA / dsDNA * Complement * Anti-PLA2R * Immunoglobulins * Rheumatoid factor * Virology – hep B, C, HIV * Others: Myeloma screen , HbA1c Kidney biopsy - confirm diagnosis

Question 32

How is a kidney biopsy carried out?

Answer 32

* Done as outpatient day case, local anaesthetic * Ultrasound used to visualise kidneys * Few samples of cortex taken (glomeruli) * Only need to take samples from one kidney - glomerulonephritis will be present in both * Usually L kidney done - easier to reach

Question 33

Why is kidney biopsy avoided where possible?

Answer 33

* Main risk = bleeding (1% risk of significant bleed requiring transfusion/embolisation to stop) * Only done when other tests will not give diagnosis

Question 34

How is a kidney biopsy used to give a diagnosis of glomerulonephritis?

Answer 34

Biopsy of kidney cortex examined under: * Light microscopy (glomerular and tubular structure) * Immunofluorescence (looking for Ig and complement) * Electron microscopy (glomerular basement membrane and deposits)

Question 35

Descrive the histological appearance of FSGS

Answer 35

Sclerotic lesions, more pink

Question 36

Describe the histological appearance of membranoproliferative glomerulonephritis

Answer 36

More purple (mesangial matrix) and mesangial cells (dark purple dots)

Question 37

Describe the clinical presentation of glomerulonephritis

Answer 37

Disruption of glomerular filtration barrier - urine abnormal (blood, protein or both) Main Presentations - Spectrum: * Incidental finding of urinary abnormalities +/- impaired kidney function * Visible haematuria * Synpharyngitic * Sore throat, urine looks like coke = classic IgA nephropathy * Nephritic syndrome * Nephrotic syndrome * Acutely unwell with rapidly progressive glomerulonephritis

Question 38

Describe the features of nephrotic syndrome

Answer 38

* 3.5g proteinuria per 24h (urine PCR \>300) * Serum albumin \<30 * Oedema (retention of salt and water) * Hyperlipidaemia (serum cholesterol 15-20)

Question 39

What are the risks associated with nephrotic syndrome?

Answer 39

* Risk of venous thromboembolism * Lose anticoagulant clotting factors through damaged glomerular BM, procoagulant state * Increased risk of infection * Lose Igs through damaged glomerular BM, risk of infection

Question 40

Describe the features of nephritic syndrome

Answer 40

* Hypertension * Blood and protein in urine * Inflammation involving endothelium * Cola-coloured urine (haematuria) * Declining kidney function

Question 41

List the causes of nephritic and nephrotic syndrome

Answer 41

* Nephritic * Crescentic GN/vasculitis * Post-infectious * IgA nephropathy (usually nephritic) * Nephrotic * Minimal change nephropathy * Membraneous nephropathy Other causes * Diabetic nephropathy * Lupus nephropathy * Membranoproliferative

Question 42

Describe the spectrum of glomerular diseases

Answer 42

* Nephrotic * Injury to podocytes * Changed architecture - scarring, depostion of matrix or other elements * Always proteinuria, sometimes haematuria * Nephritis * Inflammation * Reactive cell proliferation * Breaks in GBM * Crescent formation * Always haematuria, sometimes protein

Question 43

What is the most common primary glomerular disease?

Answer 43

IgA nephropathy - up to 1% of the normal population

Question 44

Describe the spectrum of disease in IgA nephropathy

Answer 44

* Minor urinary abnormalities * Hypertension * Renal impairment and heavy proteinuria * Rapidly progressive glomerulonephritis

Question 45

Give examples of secondary causes of IgA nephropathy

Answer 45

* May be precipitated by infection - synpharyngitic * Secondary to Henoch-Schonlein Purpura, cirrhosis, coeliac disease

Question 46

Describe the pathogenesis of IgA nephropathy

Answer 46

* Abnormal/ over-production of IgA1, IgA I/C * Mesangial IgA, C3 deposition * Mesangial proliferation * Leads to * Haematuria * Hypertension * Proteinuria (varies with prognosis) About 1/3 progress to ESRF

Question 47

How is IgA nephropathy managed?

Answer 47

* No specific therapy * Antihypertensive Rx, ACE inhibitors/ARB * Aim for BP \<125/75

Question 48

Which age group is usually affected by membraneous GN?

Answer 48

Adults

Question 49

How does membraneous GN present?

Answer 49

Nephrotic syndrome – commonest primary cause, often chronic

Question 50

What causes membraneous GN?

Answer 50

* Usually idiopathic * 10% occur secondary to malignancy, CTD, drugs, diabetes, amyloid etc

Question 51

Describe the pathology of membraneous GN

Answer 51

* Anti-phospholipase A2 receptor antibody in 70% (receptors on podocytes) * Immune complexes in basement membrane/sub-epithelial space

Question 52

Describe the natural history of membraneous GN

Answer 52

Variable * A third spontaneously remit * A third progress to ESRF over 1-2 years * A third persistent proteinuria, maintain GFR

Question 53

What are the symptoms of membraneous GN?

Answer 53

Oedema, clots, fatigue

Question 54

How is membraneous nephropathy treated?

Answer 54

* Treat underlying disease if secondary * Supportive non-immunological – ACEi, statin, diuretics, salt restriction * Tight BP control v important * Diuretics/salt for symptomatic relief of oedema * Specific immunotherapy - if not improving * Steroids * Alkylating agents (cyclophosphamide) * Alternative agents – rituximab, anti-CD20 MAb * Cyclosporin

Question 55

What are the potential outcomes of membraneous GN?

Answer 55

* Complete remission * Partial remission * ESRD * Relapse * Death

Question 56

Describe the prevalence of minimal change disease I

Answer 56

* The commonest form of GN in children * 90% of GN \< 10 years * 50% of older children * 20% of adults of all ages

Question 57

How does minimal change disease present?

Answer 57

* Nephrotic syndrome * Acute presentation - may follow URTI * GFR - normal, or reduced due to intravascular depletion * Very rarely causes renal failure * Relapsing course - 50% will relapse

Question 58

What causes minimal change disease?

Answer 58

Idiopathic but may be secondary to malignancy

Question 59

Describe the pathogenesis of minimal change disease

Answer 59

* T cell and cytokine mediated * Target - glomerular epithelial cells, GBM change

Question 60

Describe the appearance of the glomerulus on microscopy in minimal change disease

Answer 60

Glomerulus looks normal under light microscopy, can see pathology on electron microscopy * Fenestrated epithelium, podocytes w/ fingerlike processes = normal * Minimal change - podocytes fuse, can't see individual spikes

Question 61

How is minimal change disease treated?

Answer 61

High dose steroids - prednisolone 1mg/kg for up to 8 weeks

Question 62

Describe the aetiology of primary nephrotic syndrome by age

Answer 62

* Children - 90% minimal change * \<45 - minimal change, membraneous GN, fibrillary * 45-65 - membraneous GN, minimal change, fibrillary * \>65 - membraneous GN, fibrillary, minimal change/MCGN

Question 63

What is FSGS?

Answer 63

FSGS = focal segmental glomerulosclerosis * Some glomeruli affected by a scarred lesion on part of the glomerulus * Idiopathic or systemic causes * Causes nephrotic syndrome

Question 64

Describe the pathology of crescentic disease

Answer 64

* Crescent shaped expansion of inflammatory cells, necrosis, ECM around glomerulus * Active proliferative disease * Crescents heal, whole glomerulus scleroses and dies

Question 65

What is crescentic GN?

Answer 65

* Group of conditions which demonstrate glomerular crescents on kidney biopsy * Aggressive disease – progress to ESRF

Question 66

List the common causes of crescentic GN/rapidly progressive GN

Answer 66

* ANCA vasculitis (MPO / PR3) - other pathological signs e.g. rash, red eyes * Goodpasture’s syndrome (anti-GBM - antibody formed to glomerular BM) * Lupus nephritis * Infection associated - usually staphylococcal or streptococcal * HSP nephritis - IgA vasculitis

Question 67

What systemic complication is seen in ANCA vasculitis and Goodpasture's syndrome?

Answer 67

Pulmonary haemorrhages

Question 68

How can systemic diseases manifect in the kidneys?

Answer 68

* Inability to clear waste products = * Acute kidney injury * Chronic kidney disease * + inflammation * Blood - nephritic syndrome * Leakage of protein * \>3g/day, fall in serum albumin = nephrotic syndrome * Less protein leakage = proteinuria

Question 69

How is renal impairment due to systemic disease diagnosed?

Answer 69

* Renal impairment - old or new? * Previous U&E * Proteinuria? * Urinalysis & quantitative proteinuria (uPCR) * Which is it? * AKI/CKD/nephritis/nephrotic syndrome/proteinuria * Clues to systemic disease? * History and examination * Other tests * Special antibodies, complement, eosinophils, * Imaging * rRenal biopsy * Non-invasive tests first * Invasive i.e. biopsy only if needed to make Dx and will change management - higher risk

Question 70

Describe the impact of diabetes and the association with kidney disease

Answer 70

* 3.5 million diabetics in UK - estimated 4-5 million by 2025 * \>270,000 in Scotland * UK cost - £1.5 million per hour, 10% of NHS budget * 90% type 2 diabetes * 30-40% of diabetics develop kidney problems * 26% of people starting RRT are diabetic - 28% Glasgow, 15% Inverness

Question 71

How does diabetic nephropathy progress? How does this impact mortality?

Answer 71

* No nephropathy - 1.4% mortality/year * Proteinuria (micro --\> macroalbuminuria) - 4.6% mortality/year * Renal impairment - 19.2% mortality/year

Question 72

How does diabetic nephropathy usually present?

Answer 72

* Proteinuria is hallmark * Usually associated with retinopathy

Question 73

Describe the pathogenesis of diabetic nephropathy

Answer 73

1. Hyperglycaemia 2. Volume expansion 3. Intra-glomerular hypertension 4. Hyperfiltration 5. Proteinuria 6. Hypertension and renal failure Progresses over years Creatinine can go down as develop hyperfiltration - sign kidney function will decline in future

Question 74

Describe the structure changes which occur in the glomerulus in diabetic nephropathy

Answer 74

* Thickening of the glomerular BM * Fusion of podocyte foot processes * Loss of podocytes w/ wearing away of the glomerular B\< * Mesangial matrix expansion

Question 75

Describe the histology of diabetic nephropathy

Answer 75

* Pathognomic hyaline material containing nodules (excess mesangial matrix) in glomerular capillary loops * Pink nodules - Kimmelstiel-Wilson lesion

Question 76

What kidney complications occur as diabetes progresses?

Answer 76

Anaemia, bone and mineral metabolism abnormalities, retinopathy, neuropathy

Question 77

How can the risk of diabetic nephropathy be reduced?

Answer 77

* Tight glycaemic control * Best OHA or insulin regimen * Good BP control - ACEi/ARB * Targets for diabetics lower than for general population * SGLT2 - inhibitors

Question 78

Describe the mechanism of action of SGLT2 inhibitors

Answer 78

* SGLT2 channel in renal tubules reabsorbs glucose and water * SGLT2 inhibitors block reabsorption - more glucose and water excreted - lowers BG * Potentially very useful before CKD develops * Main side effect is UTIs

Question 79

Describe the cardiac/renal protection which SGLT2 inhibitors give

Answer 79

SGLT2 inhibition = * Glycosuria * Negative caloric balance --\> reduced total body fat mass --\> reduced epicardial fat (increased cardiac contractility) - less inflammation and fibrosis * Reduced HbA1c --\> less inflammation and glucose toxicity + less atherosclerosis * Increased uricosuria --\> decreased plasma uric acid --\> less atherosclerosis * Natriuresis * Lowers BP --\> less arterial stiffness * Reduced plasma volume --\> less ventricular arrhythmias, less myocardial stretch * Tubuloglomerular feedback --\> afferent arteriole constriction --\> reduced intraglomerular hypertension, reduced hyperfiltration

Question 80

How is renal artery stenosis diagnosed?

Answer 80

* Clinical diagnosis * No angiogram/CT angiogram/MRI

Question 81

Is angioplasty/stenting used in stenosed renal vessels?

Answer 81

* Unlike narrowed coronary arteries, there is evidence that angioplasty/stenting is rarely effective in renal vessels * Causes subsequent problems w/ BP, recurrent renal stenosis

Question 82

Describe the pathogenesis of renovascular disease

Answer 82

1. Progressive narrowing of renal arteries with atheroma 2. Perfusion falls by 20% - GFR falls but tissue oxygenation of cortex and medulla maintained 3. RA stenosis progresses to 70%, cortical hypoxia causes microvascular damage and activation of inflammation and oxidative pathways 4. Parenchymal inflammation and fibrosis progress and become irreversible, restoration of blood flow provides no benefit

Question 83

How is renal artery stenosis managed?

Answer 83

* Medical * BP control (not ACEi/ARB) * Statin * If diabetic, good glycaemic control * Lifestyle * Smoking cessation * Exercise * (Low sodium diet) * Angioplasty * Rapidly deteriorating renal failure * Uncontrolled ↑BP on multiple agents * Flash pulmonary oedema Treat the underlying condition

Question 84

What is amyloidosis?

Answer 84

* Deposition of highly stable insoluble proteinous material in extracellular space (felt-like substance made of beta-pleated sheets) * Numerous H-bonds through peptide amide groups make them highly stable * Kidney, heart, liver, gut * Specific ultrastructural features (8-10nm fibrils) * High affinity for the constituents of the capillary wall

Question 85

Describe the appearance of amyloidosis on microscopy

Answer 85

* Light microscopy * Congo red stain - apple green birefringence * Electron microscopy * Amyloid fibrils 9-11nm cause mesangial expansion * First deposits in mesangium, anti-GBM and BVs

Question 86

List the types of amyloidosis

Answer 86

* AA = systemic amyloidosis (inflammation/infection) * From previous chronic pyrogenic or granulomatous infections e.g. TB, familial Mediterranean fever * AL = immunoglobulin fragments from haematological condition e.g. myeloma * Ig LC λ \>κ (12:1 if renal impairment) 12ααs

Question 87

How is amyloid treated?

Answer 87

* AA amyloid - treat the underlying source of inflammation/infection * AL amyloid - treat the underlying haematological condition

Question 88

Describe the pathogenesis of systemic lupus erythematosis

Answer 88

* Auto-immune disease - immune complex mediated glomerular disease * Deposition of immune complexes * Multiple autoAbs – directed against DNA, histones, snRNPs, transcriptional/translational machinery

Question 89

Describe the epidemiology of systemic lupus erythematosis

Answer 89

* Epidemiology: * Female\>\>male (2-12:1) * African \> Asian \> Caucasian * 1 in 2500 women, 1 in 25000 men in UK

Question 90

What causes SLE?

Answer 90

Genetic predisposition (12+ genes identified) and environmental trigger

Question 91

Describe the pathophysiology of lupus nephritis

Answer 91

1. Auto-antibodies produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone) 2. Form intravascular immune complexes or attach to GBM 3. Activate complement (low C4) 4. Renal damage

Question 92

How is the diagnosis of lupus nephritis confirmed?

Answer 92

Renal biopsy - confirm diagnosis and stage disease

Question 93

How is lupus nephritis treated?

Answer 93

Immunosuppression - Steroids, MMF, cyclophosphamide, rituximab

Question 94

Describe the embryological development of the kidneys

Answer 94

* Pronephros --\> mesonephros --\> metanephros * Nephrogenesis - commences week 10 * 60% in 3rd Trimester * Premature - \>30% nephrons may not have developed * No new nephrons after 36 weeks

Question 95

Compare the renal function at birth to that of an adult

Answer 95

* Nephrons * At birth: 300 000 to 1.8 million per kidney * Mean: 895 000 * GFR : * Adult - 120mls/min/1.73m2 * At birth: 40-65mls/min/1.73m2

Question 96

How can paediatric renal function be investigated?

Answer 96

* Antenatal US * Ultrasound * MCUG – Micturating Cystourethrogram * Need to catheterise, only done in children \<1y/o * Nuclear Medicine * DMSA * MAG 3 * CT - requires general anaesthetic in children (avoided) * MR

Question 97

How prevalent are congenital anomalies of the kidney and urinary tract?

Answer 97

* 20-30% of all anomalies in prenatal period * Incidence * 1 in 500 live births * 0.3-1.6 per 1000 live or still births * Non-renal anomalies seen in 30%

Question 98

What percentage of congenital anomalies of the kidneys and urinary tract progress to CKD?

Answer 98

30-50% progress to chronic kidney disease needing RRT in children

Question 99

List the types of congenital anomalies of kidney and urinary tract

Answer 99

* Renal Dysplasia/Hypoplasia * Renal Agenesis * MCDK * Renal Cystic Dysplasia * Genetic Cystic Disease * Obstructive uropathy * Vesico-ureteric Reflux

Question 100

What is renal agenesis?

Answer 100

* Congenital absence of renal parenchymal tissue: metanephric stage * Associated with increased risk of other anomalies - structural, chromosomal

Question 101

Compare unilateral and bilateral renal agenesis

Answer 101

* Bilateral mostly sporadic, not compatible with life * Unilateral - 5% renal anomalies, prognosis - excellent

Question 102

Are males or females more commonly affected by renal agenesis?

Answer 102

Male:female = 1.7:1

Question 103

Define renal hypodysplasia

Answer 103

* Renal Hypoplasia - reduction in number of nephrons but normal architecture * Renal Dysplasia - malformed renal tissue * Renal Hypodysplasia - congenitally small kidneys with dysplastic features

Question 104

Describe the presentation of renal hypodysplasia

Answer 104

* Antenatal - US growth * Neonate - lung issues, IUGR, acidosis, raised Cr * Children - FTT, anorexia, vomiting, proteinuria

Question 105

How is renal hypodysplasia managed?

Answer 105

Supportive management

Question 106

Describe the histological appearance of a hypodysplastic kidney

Answer 106

Large glomeruli with interstital fibrosis and foci of atrophic tubules

Question 107

How is a multicystic dysplastic kidney detected?

Answer 107

* Antenatal - US * Neonatal - abdominal mass

Question 108

What percentage of multicystic dysplastic kidneys spontaneously involute?

Answer 108

35-65%

Question 109

What risks are associated with a multicystic dysplastic kidney?

Answer 109

* Hypertension * Malignancy - risk now same as general population

Question 110

List the types of genetic cystic disease

Answer 110

* Autosomal recessive polycystic kidney disease * Autosomal dominant polycystic kidney disease

Question 111

Describe the clinical presentation of autosomal recessive polycystic kidney disease

Answer 111

* Antenatal: * Antenatal US * Oligohydramnios * Infancy: * Large palpable renal mass * Respiratory distress * Renal failure - HT * Hyponatremia - urinary concentrating defect * Childhood: * Renal failure * HT

Question 112

Describe the histopathology of autosomal recessive polycystic kidney disease

Answer 112

Cystic dilatations of the collecting tubules w/ flattening of the epithelium that runs perpendicular to the renal capsule

Question 113

What anomalies are associated with autosomal recessive polycystic kidney disease?

Answer 113

* Congenital Hepatic Fibrosis - subclinical to liver disease * Portal HT * Ascending cholangitis

Question 114

Describe the prognosis of autosomal recessive polycystic kidney disease

Answer 114

* 20-30% mortality in neonatal period * 5yr survival: 70-88% * Progression to ESRF over 50%, often \>15yrs * 30-50% in 10yrs

Question 115

Describe the incidence of autosomal dominant polycystic kidney disease

Answer 115

1 in 500-1000

Question 116

Describe the genetic causes of autosomal dominant polycystic kidney disease

Answer 116

* PKD1 mutation – cc 16: 85%, polycystin 1 * PKD2 mutation – cc 4: 10-15%, polycystin 2 * 5-10% new mutation

Question 117

What is seen on ultrasound in autosomal dominant polycystic kidney disease?

Answer 117

* Large echogenic kidneys * Macrocysts * Infancy - occasional * Older chold - multiple * Pathology * Cysts originating from tubules

Question 118

Describe the clinical presentation of autosomal dominant polycystic kidney disease

Answer 118

* Antenatal: * Antenatal US * Childhood: * Haematuria * HT * Flank pain * UTIs * Renal US - may be unilateral * Adult: * Majority of presentations * Renal US: often 2nd-3rd decade * HT * Haematuria * Family History

Question 119

List the anomalies associated with autosomal dominant polycystic kidney disease

Answer 119

* Mitral valve prolapse * Cerebral Aneurysm * AV malformation * Hepatic/pancreatic cysts * Colonic diverticula/hernia

Question 120

How autosomal dominant polycystic kidney disease managed?

Answer 120

* Supportive * Directed - Tolvaptan

Question 121

Describe the prognosis of autosomal dominant polycystic kidney disease

Answer 121

* Progression to ESRF in adulthood * 50% by 60 yrs

Question 122

Are males or females more commonly affected by hydronephrosis?

Answer 122

Males:females = 2:1

Question 123

What percentage of hydronephrosis is bilateral?

Answer 123

20-40%

Question 124

What are the consequences of hydronephrosis?

Answer 124

Associated with renal injury and impairment

Question 125

How can hydronephrosis be diagnosed antenatally/postnatally?

Answer 125

* Antental - AP diameter, can be transient * Postnatal ultrasound - renal pelvic diameter \>10mm

Question 126

What can cause hydronephrosis?

Answer 126

Vesico-ureteric reflux Obstruction of the urinary tract

Question 127

Describe the levels of obstruction of the urinary tract

Answer 127

* Pelvis/ureter - pelvic-ureteric junction * Ureter * Ureter/bladder - vesico-ureteric junction * Bladder * Urethra

Question 128

Define urinary obstruction

Answer 128

Impedance to urinary flow which causes gradual/progressive change

Question 129

How common is PUJ obstruction?

Answer 129

1 in 500 births Males \> females Bilateral 10%

Question 130

Define PUJ obstruction

Answer 130

Partial/total blockage of urine at ureter junction with kidney

Question 131

How does PUJ obstruction present?

Answer 131

* Antenatal diagnosis * Abdominal mass * UTI * Failure to thrive * Abdominal/flank pain

Question 132

Define VUJ obstruction?

Answer 132

* Functional/anatomical abnormality at vesico-ureteric junction * --\> megaureter * Primary - reflux/obstruction * Secondary - bladder issues * Ureteric dilatation \>7mm

Question 133

Describe the prevalence of primary VUJ obstruction

Answer 133

* 2nd most common neonatal hydronephrosis - 20%

Question 134

Describe the incidence of obstruction of the posterior urethral valves

Answer 134

* Most common obstructive uropathy * 1 in 4-8000 births

Question 135

How does posterior urethral valve obstruction present?

Answer 135

* Antenatal detection * Bilateral hydronephrosis * UTI

Question 136

What investigations are done to diagnose posterior urethral valve obstruction?

Answer 136

US, MCUG

Question 137

What are the complications associated with posterior urethral valve obstruction?

Answer 137

Risk of CKD, bladder dysfunction Continence problems - catheterisation

Question 138

Define vesico-ureteric reflux

Answer 138

Retrograde passage of urine from bladder into upper urinary tract

Question 139

What are the complications associated with vesico-ureteric reflux?

Answer 139

* UTIs leading to scarring * Hypertension * ESRF

Question 140

How prevalent is vesico-ureteric reflux?

Answer 140

1% births

Question 141

How is vesico-ureteric reflux diagnosed?

Answer 141

MCUG

Question 142

How is vesico-ureteric reflux classified?

Answer 142

* Grades I-V * V - into calyx, dilating ureter * Grades 1-3 usually resolve spontaneously

Question 143

Describe the prevelance of UTIs in children

Answer 143

* Prevalence \<1-16% in under 2 yrs, 8% in older children * Girls\> Boys – unless \<3 months * Variable - age, gender, race, circumcision status

Question 144

Define significant bacteriuria

Answer 144

* \>10^5 colony forming units/ml * Single pathogenic bacteria

Question 145

How is urine collected from children?

Answer 145

* Difficult in young children * Clean catch urine sample * Mid-stream sample of urine * Catheter specimen * Supra-pubic aspirate

Question 146

What is the most common causative agents of UTIs in children?

Answer 146

* E Coli (\>80%) * Other organisms: Klebsiella/Pseudomonas * Associated w/ abnormalities in urinary tract

Question 147

List the risk factors for UTIs in children

Answer 147

* Age * Circumcision - unlikely to get UTIs * Urinary Obstruction * Vesico-ureteric Reflux * Bladder/bowel dysfunction * Catheterisation * Sexual activity

Question 148

Describe the clinical presentation of UTIs in children

Answer 148

* Upper Tract * Pyrexia (Rigors) * Vomiting * Systemic upset * Abdominal pain * Lower Tract * Dysuria * Frequency * Haematuria * Wetting

Question 149

What investigations should be done to diagnose UTIs in children?

Answer 149

* Urine dip + culture * Associated w/ underlying anomalies and can lead to scarring/HT/ESRF * Ultrasound * MCUG * Nuclear medicine

Question 150

Define Von Hippel Lindau

Answer 150

* Rare * Autosomal dominant * Multisystem - kidneys, pancreas and genital tract * Multiple cysts - benign w/ potential for malignant transformation (clear cell carcinoma) * Tumours tend to appear in early adulthood

Question 151

Define tuberous sclerosis

Answer 151

* Autosominal dominant * Multisystem, benign tumours - brain, kidneys, heart, eyes, skin * Kidneys - tumours called angiomyolipomas * Seizures, developmental delay * Risk of haemorrhage * Rarely progress to ESRD

Question 152

Define medullary cystic disease

Answer 152

* Autosomal dominant * Cystic in medulla not cortex * Tubulo-interstitial fibrosis * Small to normal sized kidneys * Usually results in ESRD

Question 153

Compare the PKD1 and PKD2 mutations in adults polycystic kidney disease

Answer 153

* PKD 1 gene mutation (chromosome 16) = 85% (1270 mutations). Typical rapid progression with ESRD \< 50yrs * PKD 2 gene mutation (chromosome 4) = 15% (200 mutations). Slower progression, may never reach ESRD * 10-25% - no family history (new mutations)

Question 154

How prevalent is adult polycystic kidney disease?

Answer 154

* 10% RRT patients in UK * Prevalence 1/1000

Question 155

How do the polycystin gene mutations cause adult polycystic kidney disease?

Answer 155

* Genes code for polycystin 1 and 2 * Polycystins are located in renal tubular epithelia * Membrane proteins - kidneys, brain, heart, bone, muscles, liver and pancreas ducts * Overexpressed in cyst cells * Membrane proteins involved in intracellular calcium regulation * Mechanism of cyst formation poorly understood

Question 156

Describe the presentation of adult polycystic kidney disease

Answer 156

* Presentation variable – incidental finding on USS, HTN, impaired renal function, loin pain, haematuria, mass on examination * Cysts gradually enlarge, normal kidney tissue replaced. Kidney volumes increased and eGFR falls * ESDR within 5-10 years * Cyst infection, cyst rupture, haematuria, pain

Question 157

Describe the extra-renal manifestations of adult polycystic kidney disease

Answer 157

* Intracranial aneurysms, arachnoid cysts * If FH - screened for aneurysm * Cardiac - HTN, LVH, valvular abnormalities * Hepatic and pancreatic cysts * Bronchiectasis * Diverticular disease, abdominal hernias

Question 158

How is adult polycystic kidney disease diagnosed?

Answer 158

* Ultrasound * Differentiate between ‘simple renal cysts’ * Over 70y, 10% of patients will have cysts in both kidneys and 22% will have at least one kidney cyst * Family history – ultrasound at age 21 (if negative, should be repeated age 30 or will miss 14%) * Age 15-30 : 2 unilateral or bilateral cysts * Age 30-59: 2 cysts in each kidney * Over age 60: 4 cysts in each kidney * No family history: 10 or more cysts in both kidneys, renal enlargement, liver cysts * CT or MRI more sensitive * Genetic testing - only identifies 70% mutations * Not for screening, useful in abnormalities on US or in potential kidney donors

Question 159

How is adult polycystic kidney disease managed?

Answer 159

* Management is supportive * Early detection and management of blood pressure * High BP - renal function more likely to deteriorate faster * Treat complications * Manage extra-renal associations * Prepare for renal replacement therapy * Recent development * Tolvaptan - used for hypernatraemia * Suppresses effects of vasopressin - key in kidney cyst formation

Question 160

Describe the use of tolvaptan in practice

Answer 160

* Delay onset of RRT by around 4-5 years * Intensive monitoring – monthly LFTs for 18 months * Side effects of hepatotoxicity, hypernatraemia * Polyuric - 6-8L of urine per day, have to drink that amount * High rate of discontinuation in a 3 year trial (23% vs. 14%) * Expensive * Recommended for use by Scottish medicines consortium (SMC) for CKD3 and declining renal function

Question 161

Describe the inheritance of Alport's syndrome

Answer 161

Usually X-linked if inherited - affected or carrier

Question 162

Describe the prevalence of Alport's syndrome

Answer 162

Second most common inherited kidney disease (1/5000 prevalence)

Question 163

Describe the mutation which causes Alport's syndrome

Answer 163

Collagen 4 abnormalities- alpha 3 gene mutation, alpha 4 gene (COL3A4) mutation or alpha 5 (COL3A5) gene mutation

Question 164

Describe the presentation of Alport's syndrome

Answer 164

* Deafness * Hearing normal at birth but develop high tone hearing loss * Renal failure

Question 165

Describe the histological appearance of Alport's syndrome

Answer 165

* Collagen 4 deposition at basement membranes * Basement membrane thinning and thickening - abnormally split and laminated = basket weave appearance

Question 166

Describe the clinical consequences of Alport's syndrome

Answer 166

* Microscopic haematuria, proteinuria and end stage renal failure (ESRF) * 90% on dialysis or transplant by age 40y, 50% by age 25y * Sensorineural hearing loss late childhood * Female Alport’s carriers – 12% ESRF by age 40y

Question 167

Define Fabry's disease

Answer 167

* X-linked storage disorder * Alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)

Question 168

Describe the prevalence of Fabry's disease

Answer 168

Rare 1/40,000

Question 169

Describe the pathogenesis of Fabry's disease

Answer 169

* Gb3 accumulates in glomeruli, particularly podocytes causing proteinuria and ESRF – average age of onset 34y * Also causes neuropathy, cardiac and skin features

Question 170

How is Fabry's disease diagnosed?

Answer 170

* Measure alpha-Gal A activity in leukocytes * Renal biopsy – inclusion bodies of G3b

Question 171

How is Fabry's disease managed?

Answer 171

Enzyme replacement therapy

Question 172

Describe the appearance of IgA nephropathy on immunofluorescence

Answer 172

IgA deposits in mesangium

Question 173

Define Henoch-Scholein purpura

Answer 173

* Often paediatric condition * Multisystemic vasculitis * Purpuric rash on buttocks and backs of legs * Immune reaction mediated by IgA causing deposition in blood vessels systemically

Question 174

What does a positive cANCA and high PR3 antibody level suggest?

Answer 174

ANCA associated vasculitis = Granulomatosis with polyangiitis

Question 175

What can be seen on CXR in ANCA associated vasculitis?

Answer 175

Acute pulmonary haemorrhage

Question 176

What does a positive MPO suggest?

Answer 176

Eosinophilic granulomatosis with polyangiitis (Goodpasture's syndrome)

Question 177

Describe the systemic effects of granulomatosis with polyangiitis

Answer 177

* Oral cavity - ulcerations throughout oral mucosa * Lungs - cavities, bleeds, lung infiltrates * Skin - nodules on the elbow, purpura * Granulomas and patchy necrosis in blood vessels * Eye - pseudotumours, conjunctivities * Nose - stuffiness, noseblees, saddle nose * Heart - pericarditis * Kidneys - glomerulonephritis * Positive anti-neutrophil cytoplasm test

Question 178

Describe the mortality associated with AKI

Answer 178

* Overall mortality for patients with AKI requiring dialysis is 20-30% * Additional mortality due to sepsis, bleeding, respiratory failure etc.

Question 179

Define AKI

Answer 179

UKRA guidelines - decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatinine

Question 181

How is the severity of AKI graded?

Answer 181

KDIGO * Stage 1: Serum creatinine ≥1.5 and \< 2.0 times AKI baseline or \>=26.0 µmol/l increase above AKI baseline * Stage 2: Serum creatinine \>=2.0 and \< 3.0 times AKI baseline * Stage 3: Serum creatinine 3.0 times AKI baseline or \>=354 µmol/l increase above AKI baseline

Question 182

Define oliguric vs non-oliguric AKI

Answer 182

* Oliguria -urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults * Gives some clues with diagnosis * Non-oliguric easier to manage, both serious

Question 183

Describe AKI e-Alerts

Answer 183

Highlight AKI using lab algorithm - widely used * Calculated - not required knowledge * Serum creatinine \>1.5 times higher than the median of all creatinine values 8-365 days ago * Serum creatinine \>1.5 times higher than the lowest creatinine within 7 days * Serum creatinine \>26 umol/L higher than the lowest creatinine within 48 hours

Question 184

How is AKI classified diagnostically?

Answer 184

* Pre-renal - circulatory failure 'shock' * Renal - cells of the kidney * Post-renal - obstruction

Question 185

List the pre-renal causes of AKI

Answer 185

Anything that impairs renal perfusion * Hypotension * Hypovolaemia (burns, diarrhoea, haemorrhage etc) * Hypoperfusion * hypoxia * Sepsis (vasodilation so effective perfusion ↓) * Drugs, toxins

Question 186

List the post-renal causes of AKI

Answer 186

Obstructive causes - anything between renal pelvis and urethral meatus which obstructs flow of urine * Calculi * Tumours (ureter, bladder, prostate, cervix, ovarian, can be extrinsic) * Lymph nodes (compression) * Prostate

Question 187

What are the most common post-renal causes of AKI in women and men?

Answer 187

Men - prostate Women - gynaecological tumours

Question 188

List the most common causes of AKI

Answer 188

* Acute tubular necrosis 80% * Obstructive 10% * Glomerulonephritis (primary and secondary) - 3% * Acute tubulointerstitial nephritis 2% * Vasculitis 1.5% * Atheroembolic 1% * Other 2.5%

Question 189

List the renal causes of AKI

Answer 189

* Glomeruli (vasculitis) - glomerulonephritis, drugs (e.g. gentamicin) * Tubules - tubulo-interstitial nephritis, rhabdomyolysis

Question 190

Describe the impact of acute tubular necrosis on renal function

Answer 190

* Usually reversible * 10-15% never recover renal function * Further 10-15% have chronic renal impairment

Question 191

What causes acute tubular necrosis?

Answer 191

Under perfusion of tubules and/or direct toxicity * Hypotension * Sepsis * Toxins Or often, all three

Question 192

List the exogenous and endogenous toxins which can cause acute tubular necrosis

Answer 192

* Exogenous * Drugs e.g. NSAIDs, gentamicin, ACE inhibitors * Contrast * Poisons e.g. metals, antifreeze * Endogenous * Myoglobin * Haemoglobin * Immunoglobulins * Calcium * Urate

Question 193

Describe the physiological response in glomerular filtration to decreased pressure

Answer 193

Prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80mmHg

Question 194

Describe the immediate assessment of AKI

Answer 194

* Acute or chronic * Bloods - both urea and creatinine high * Potassium * Urine output (usually \<400ml/day) * Clinical assessment of fluid status (BP, JVP, oedema, heart sounds) * Underlying diagnosis - history, examination, medications

Question 195

Describe the immediate treatment of AKI

Answer 195

* Immediate * Airway and Breathing * Circulation – shock - restore renal perfusion * Hyperkalaemia * Pulmonary oedema * Remove causes * Drugs * Sepsis * Exclude obstruction & consider ‘renal’ causes * Are the pre-renal causes sufficient to account for AKI? * Ask for help: ICU or renal unit

Question 196

Describe the diagnostic process in AKI

Answer 196

Need for urgent action may take precedence over making final diagnosis * AKI or CKD? * History and exam e.g. septic, rashes, haemoptysis, rhabdomyolysis etc. * Drugs - prescribed, OTC, supplements, radio-contrast and abuse * Urinalysis * GN screen - ANCA, ANA, immunoglobulins + EP, complement, aGBM, urine Bence Jones protein * Others blood film, LDH, CK etc.

Question 197

How can obstruction be excluded in AKI?

Answer 197

* Renal US * Also gives info on size (small in CKD) * Loss of corticomedullary differentiation suggests CKD

Question 198

What levels of serum potassium are considered clinically relevant?

Answer 198

K \<6.0 - abnormal but no immediate concern K 6.0-6.4 - risk of arrhythmia, needs treatment esp. if ECG changes K \>6.5 - medical emergency

Question 199

Describe the treatment of hyperkalaemia in AKI

Answer 199

* Reduce absorption from gut – Calcium Resonium 15g 4x day orally (or enema), new drugs coming * Insulin 10-15units actrapid + 50ml 50% dextrose moves potassium into cells (watch BM) * Calcium gluconate 10ml 10% as cardiac membrane stabiliser

Question 200

How is acidosis treated in AKI?

Answer 200

* If raised potassium and HCO3 \<16 also worth bicarb supplementation * IV NaBicarb 1.26%

Question 201

What are the indications (absolute and relative) for dialysis in AKI?

Answer 201

Absolute Indications for Dialysis: * Refractory potassium \>6.5 mmol/l * Refractory pulmonary oedema Relative indications for Dialysis: * Acidosis (pH \<7.1) * Uraemia (esp if urea \>40) * Pericarditis, encephalopathy * Toxins (lithium, ethylene glycol etc.)

Question 202

Describe the outcomes in AKI

Answer 202

* Dialysed for AKI- mortality 20-30% (often in ITU) * 85% return to baseline kidney function * 10% are left with some renal impairment * 5% do not recover kidney function i.e. need long term dialysis or transplant

Question 203

Describe the recovery of the kidneys from ATN

Answer 203

* Often a polyureic phase for 48-72hr * May be up to 6l urine/day * Often subsequent low K, Ca, Mg as ‘low quality' urine * Tubules fail to concentrate urine

Question 204

Define chronic kidney disease

Answer 204

CKD = kidney damage or GFR \<60 ml/min per 1.73m2 for 3 months or more

Question 205

What are the problems with using serum creatinine to calculate eGFR?

Answer 205

Exponential relationship leads to: * Slow recognition of loss of the first 70% of renal function i.e. LAG TIME * Surprise at the sudden rise in creatinine with late renal referral Effect of muscle mass leads to: * Overestimation of function in women * Overestimation of function in the elderly * Overestimation in other low muscle mass groups e.g. amputees, para/quadriplegics, rheumatoid arthritis

Question 206

List the problems with using eGFR as a measurement of kidney function

Answer 206

* Only validated in whites and African-Americans * Mean age 50 - not validated in elderly * Values above 60ml/min not distinguishable so reported as eGFR \>59ml/min * Drug dosing - doesn't take weight into account * AKI - not valid * Pregnancy

Question 207

When can proteinuria be seen in a healthy patient?

Answer 207

After exercise, fever

Question 208

Describe normal ACR, PCR and albuminuria

Answer 208

* Normal ACR \<2.5 * Normal PCR \<20 * Albuminuria ACR \>30 * ACR is about 2/3 of equivalent PCR result * E.g. ACR 70 = PCR 100 = 24h urine protein 1g * Nephrotic range proteinuria: PCR \>300 (3g/24 hour) * If heavy albuminuria use PCR to follow progress

Question 209

List the signs and symptoms of advanced CKD

Answer 209

* Symptoms: * Pruritus * Nausea, anorexia, weight loss * Fatigue * Leg swelling * Breathlessness * Nocturia * Joint/bone pain * Confusion * Signs: * Peripheral and pulmonary oedema * Pericardial rub * Rash/excoriation * Hypertension * Tachypnoea * Cachexia * Pallor &/or lemon yellow tinge

Question 210

Describe the general principles of CKD

Answer 210

* Targeted screening for CKD * Interventions to slow the rate of progression of CKD and reduce cardiovascular risk * Medicines to replace impaired individual functions of the kidney * Advanced planning for future renal replacement therapy (RRT) * Renal replacement therapy

Question 211

How can you slow the rate of progression of CKD?

Answer 211

* Aggressive BP control * Good diabetic control * Diet * Smoking cessation * Lowering cholesterol * Treat acidosis

Question 212

Which drugs should be used for BP control in CKD?

Answer 212

* ACEI/ARB drugs of choice for hypertension in CKD if * All BP lowering will reduce rate of progression * Reduction in eGFR of up to 25% in first few weeks is good * Will get more of a reduction if critical reduced renal perfusion (volume depletion, sepsis, RAS)

Question 213

How is anaemia managed in CKD?

Answer 213

* Replace iron, B12, folate first if low * ESA e.g. Darbepoetin alfa 30microg every 2 weeks * Trigger usually Hb \<100g/l * Target Hb 100-120g/l. * Higher associated with adverse CV events

Question 214

Describe the pathophysiology of secondary hyperparathyroidism in CKD

Answer 214

* CKD - low activated vitamin D, phosphate not excreted properly so high serum phosphate * Insoluble calcium phosphate forms and removes calcium from circulation * Leads to hypocalcaemia --\> secondary hyperparathyroidism * Secondary hyperparathyroidism - muscle aching/weakness, bone pain

Question 215

How is metabolic bone disease in CKD treated?

Answer 215

* Activated vitamin D - Alfacalcidol, start 0.25mcg * Occasionally Mg supplements * Phosphate binder - target phosphate 0.9-1.5 mmol/l * Calcium based - calcium carbonate/acetate * Non-calcium - sevelamer, lanthanum, aluminium * Calcimimetic - cinacalcet * Parathyroidectomy

Question 216

When should dialysis be started in CKD?

Answer 216

* Individual approach based on symptoms * Most start with eGFR 6-8ml/min * No benefit to early start * Weight loss and persistent nausea * Persistent hyperkalaemia, acidosis, severe hyper-phosphataemia or pruritis * Problematic fluid overload * Best to have permanent access

Question 217

What are the indications to commence RRT?

Answer 217

1. Medically resistant hyperkalaemia 2. Medically resistant pulmonary oedema 3. Medially resistant acidosis 4. Uraemic pericarditis 5. Uraemic encephalopathy & specific drug overdoses

Question 218

Describe the symptoms of clinical uraemia

Answer 218

* Anorexia * Vomiting * Itch * Restless legs * Weight loss * Metallic taste

Question 219

At what level of GFR should RRT be commenced?

Answer 219

* No absolute rule * Generally eGFR between 5-10ml/min/1.73m2 * Assessed on individual patient basis

Question 220

What are the options for RRT?

Answer 220

* Haemodialysis * Hospital vs home * Daily vs nocturnal * Peritoneal dialysis * CAPD vs APD * Daily vs nocturnal * Renal transplant * Cadaveric vs living * Other - SPK, pre-emptive, altruistic

Question 221

Describe the aims of haemodialysis

Answer 221

* Removal of solutes e.g. potassium, urea = diffusion * Removal of fluid 'ultrafiltration' - pressure = hydrostatic filtration

Question 222

Describe the process of haemodialysis

Answer 222

* Blood out * Diffusion removes solutes * Filtration removes fluid * Dialysate discarded * Blood in

Question 223

Describe the options for haemodialysis

Answer 223

* Tunnelled central venous catheter --\> superior vena cava --\> right atrium of heart * Arteriovenous fistula - graft between vein and artery

Question 224

How is haemodialysis carried out in practice?

Answer 224

* Hospital or home based - hospital much more common * Standard - 4h, 3x per week * Multiple other options - mainly home based * 6h 3x per week * Short daily dialysis * Daily overnight * Home based treatment gives greater flexibility and empowerment but need carer, space and capital investment

Question 225

What are the complications of haemodialysis?

Answer 225

* 'Crash’ (acute hypotension) * Access problems * Cramps * Fatigue * Hypokalaemia * Blood loss * Dialysis disequilibrium * Air embolism

Question 226

Describe the process of peritoneal dialysis

Answer 226

* 2-3L of dialysis fluid into abdomen * Waste products (urea, creatinine) diffuse across peritoneum from underlying blood vessels * 4-6 hours later fluid removed and replaced with fresh fluid * Fluid contains sodium chloride, lactate or bicarbonate and a high percentage of glucose to ensure hyperosmolarity - drives filtration of fluid by osmosis from peritoneal capillaries to peritoneal cavity (glucose into peritoneal capillaries)

Question 227

How is peritoneal dialysis carried out in practice?

Answer 227

* Home-based therapy * Better with some residual renal function * Different glucose concentrations of dialysate to provide more or less ultrafiltration * Dialysate contains other electrolytes like in HD * Gradual treatment - no good for AKI * Simple procedure once taught * Maintain independence

Question 228

What are the complications of peritoneal dialysis?

Answer 228

* Infection - peritonitis * Glucose load – development or worsening control of diabetes * Mechanical – hernia, diaphragmatic leak, dislodged catheter * Peritoneal membrane failure * Hypoalbuminaemia * Encapsulating peritoneal sclerosis

Question 229

Which patients are not suitable for peritoneal dialysis?

Answer 229

* Grossly obese * Intra-abdominal adhesions * Frail * Home not suitable

Question 230

What are the options other than RRT in CKD?

Answer 230

* Conservative care * Increasingly frail and elderly population * Survival may be better on RRT but quality of life may not * Symptom based management

Question 231

What considerations should be made when choosing the modality of RRT?

Answer 231

* Lifestyle * Frailty * Vascular access * Time – travel to and from hospital * Carer * Physical – concurrent medical problems e.g. disseminated malignancy, severe dementia, severe psychiatric disease

Question 232

What problems in CKD are not helped by dialysis?

Answer 232

* Anaemia * Need erythropoesis supplementing agents and iron * Renal bone disease * Need phosphate binders and vitamin D * Neuropathy * Endocrine disturbances Dialysis only gives around 10ml/min eGFR - not as good as transplant

Question 233

How long do patients have to wait for cadaveric kidney transplants?

Answer 233

* Cadaveric waiting list * Kidney after brainstem death * Kidney after cardiac death * Average wait 3 years

Question 234

Describe the pros and cons of kidney transplantation

Answer 234

* Pros * No dialysis * Better level of renal function * Can live much more independently * Better life expectancy * Fertility better * Cons * Immunosuppressive medication for duration of transplant * Increased cardiovascular risk * Increased infection * Post transplant diabetes * Skin malignancies and others

Question 235

Define bacteriuria

Answer 235

Bacteria in urine

Question 236

Give examples of lower urinary tract infections

Answer 236

Cystitis

Question 237

Give examples of upper urinary tract infections

Answer 237

Pyelonephritis, renal abscess

Question 238

What is an uncomplicated vs complicated UTI?

Answer 238

* Uncomplicated UTI * Lower UTI, normal structure & neurology * Complicated UTI * UUTI +/- systemic signs and symptoms * CAUTI - catheter associated urinary tract infection

Question 239

What is a relapsed UTI vs recurrent UTI

Answer 239

Relapse = infection w/ same organism Recurrent = infection w/ same or different organism

Question 240

Define urosepsis

Answer 240

Complicated UTI * Temp \>38 * HR \>90 * RR \>20 * WBC \>15.0 or \<4.0

Question 241

Describe the prevalence of bacteruria and groups at high risk

Answer 241

* Preschool age, girls \> boys * Adults * Non-pregnant females, 1-3% * Males 0.1% * Other at risk groups * Hospitalised * Catheterised * Diabetics * Anatomical abnormalities * Pregnant

Question 242

How is bacteriuria managed?

Answer 242

* Treat asymptomatic bacteriuria only in * Preschool children * Pregnancy * (Renal transplant) * (Immunocompromised) * Treatment in other asymptomatic not indicated

Question 243

Describe the types of urinary tract infections

Answer 243

* Ascending * Urethral colonisation * F\>M * Multiplication in bladder --\> ureteric involvement * Descending/haematogenous * Blood-borne infections * Involvement of renal parenchyma

Question 244

Are urinary tract infections usually caused by a single organism or multiple?

Answer 244

* \>95% caused by single organism * Multiple organisms in * Long term catheters * Recurrent infection * Structural/ neurological abnormalities

Question 245

In which cases are multi-drug resistant organisms seen in UTIs?

Answer 245

* Anatomical/neurological abnormalities * Frequent infections * Multiple antibiotic courses * Prophylactic antibiotic use Increasing prevalence of carbapenem resistant organisms - ESBL, Amp C

Question 246

List the clinical features of urinary tract infections

Answer 246

* Suprapubic discomfort * Dysuria * Urgency * Frequency * Cloudy, blood stained, smelly urine * Low-grade fever * Sepsis * Failure to thrive, jaundice in neonates * Abdominal pain and vomiting in children * Nocturia, incontinence, confusion in the elderly

Question 247

List the common organisms which cause urinary tract infections

Answer 247

* Gram -ve bacilli * E coli * Klebsiella sp. * Proteus sp. * Pseudomonas sp. * Gram +ve bacteria * Streptococcus sp. * S agalactiae (group B strep) * Enterococcus sp. * Staphylococcus sp. - S saphrophyticus, S. aureus * Anaerobes * (Candida sp.)

Question 248

What investigations/treatment should be done in non-pregnant women with uncomplicated UTIs?

Answer 248

* 1st presentation - culture not mandatory * Dipstick, high false positive rate * Check previous culture results * Antibiotic 3-7/7 * No response to treatment * Urine culture * Change antibiotic

Question 249

How should children/men with uncomplicated UTIs be investigated/managed?

Answer 249

* Send urine for culture every presentation * Treat appropriately

Question 250

How should an uncomplicated UTI in pregnancy be investigated/managed?

Answer 250

* Common * Send urine sample w/ every presentation * Treat for 7-10 days * Amoxicillin and cefalexin relatively safe * Avoid trimethoprim in 1st trimester * Avoid nitrofurantoin near term * May need hospital admission for IV if severe * Can develop into pyelonephritis (30%)

Question 251

Define recurrent UTIs

Answer 251

* \>2 episodes in 6 months * \>3 episodes/year * Mostly women

Question 252

How are recurrent UTIs investigated/managed?

Answer 252

* Send urine sample w/ each episode * Urology investigation * Encourage hydration, urge initiated + post coital voiding * Intravaginal/oral oestrogen * Self administered single dose/short course therapy * Single dose post coital abx * Prophylactic antibiotics * If simple measures fail * Ideally 6 months * Trimethoprim * Nitrofurantoin * Associated risk w/ long term use * Development of antimicrobial resistance

Question 253

Describe catheter associated UTIs

Answer 253

* Colonisation of catheters common - treatment not required * Hospital associated infection, 35% * Disturbance of flushing system * Colonisation of urinary catheter * Biofilm production by bacteria * Likely organisms * Patient's flora * Healthcare environment

Question 254

What complications are associated with catheters?

Answer 254

* CAUTI * Obstruction-hydronephrosis * Chronic renal inflammation * Urinary tract stones * Long term risk of bladder cancer

Question 255

How can catheter infections be prevented?

Answer 255

* Catheterise only if necessary * Remove when no longer needed - 'forgotten catheter' * Remove/replace if causing infection * Catheter care (bundles) * Hand hygiene

Question 256

How is CAUTI treated?

Answer 256

* Check recent/previous microbiology * Start empirical antibiotics * Remove catheter if not needed * Replace catheter under antibiotic cover * Historically Gentamicin/Ciprofloxacin * Poor gram -ve cover * Increase in resistant GNB - treatment failure * May need broad spectrum

Question 257

What is acute pyelonephritis?

Answer 257

* Upper UTI * Moderate --\> severe * Ascending infection involving renal pelvis * Enlarged kidney w/ abscesses on surface

Question 258

How is acute pyelonephritis treated?

Answer 258

* Check previous/recent microbiology results * Send urine +/- blood culture +/- imaging * Community - co-amoxiclav/ciprofloxacin/trimethoprim (NICE) * Options may be limited * Allergy * Drug interaction * Antimicrobial resistance * Hospital - often broad spectrum abx * May remain symptomatic for few days * No response warrants further investigation * Uncomplicated pyelonephritis, 7-14/7 antibiotic * Complicated pyelonephritis, \>14/7 therapy * +/- radiological/surgical intervention

Question 259

What is the long term complication of acute pyelonephritis?

Answer 259

Renal abscess

Question 260

What is a renal abscess?

Answer 260

* Complication of pyelonephritis * Similar symptoms to pyelonephritis * Usually positive urine and blood culture

Question 261

What is the likely causative organism in renal abscesses?

Answer 261

Gram negative bacilli

Question 262

What is the life threatening complication of a renal abscess?

Answer 262

Emphysematous pyelonephritis - need urgent urology review, high mortality rate

Question 263

What are the risk factors for a perinephric abscess?

Answer 263

* Untreated LUTI, anatomical abnormalities * Renal calculi * Bacteraemia, haematogenous spread

Question 264

What are the common causative organisms of a perinephric abscess?

Answer 264

* Gram negative bacilli - E. Coli, Proteus sp. * Gram positive cocci, S. Aureus, streptococci * Candida sp.

Question 265

What are the symptoms of a perinephric abscess?

Answer 265

* Similar to pyelonephritis * Localised signs/symptoms * Usually positive blood cultures * Pyuria +/- bacterial growth

Question 266

How are perinephric abscesses managed?

Answer 266

* Treat empirically as complicated UTI * Poor response to antibiotic therapy * Surgical management

Question 267

How should all patients be investigated in complicated UTIs?

Answer 267

* FBC, U+Es, CRP * Urine sample * Urethral, CSU, Suprapubic, Nephrostomy * Blood culture if pyrexia or hypothermic * Renal ultrasound * CT KUB * Antibiotic therapy 14/7 or more

Question 268

How are urine microscopy results interpreted?

Answer 268

* Epithelial cells, contamination * Bacteria with no WBC, contamination * Bacteria with WBC and no catheter, infection * Bacteria with WBC + catheter, assess clinically * Pyuria with no bacteria * Previous/recent antibiotic * Tumour * Calculi * Urethritis (check for Chlamydia) * Tuberculosis

Question 269

Describe the antibiotic guidelines for UTIs

Answer 269

* Empirical cover * Check previous/recent microbiology * Check drug interaction and allergies

Question 270

Describe antibiotic treatment of an uncomplicated UTI

Answer 270

PO amoxicillin, trimethoprim, nitrofurantoin, pivmecillinam, fosfomycin (co-amoxiclav, ciprofloxacin, cefalexin)

Question 271

Describe antibiotic treatment of a complicated UTI

Answer 271

* Usually IV * Amoxicillin/vancomycin * Gentamicin/Aztreonam/Temocillin * Many not be suitable for all patients * Resistant organisms, ESBL, Amp C producers * Contraindications e.g. renal failure * Drug monitoring may be needed e.g. Gentamicin * Different antibiotics have different activities * Do not omit an antibiotic without finding an alternative

Question 272

What are the problems caused by multi-drug resistant bacteria in UTIs?

Answer 272

* Selection pressure of antibiotic use - development of resistant bacteria * Simple UTIs unmanageable in community * Out-Patient Parenteral Antimicrobial Therapy (OPAT) * For some patients, very little left * Hospital admission and risk of HAIs * Morbidity/mortality * Bed occupancy * Cost

Question 273

What causes acute bacterial prostatitis?

Answer 273

* Usually spontaneous * May follow urethral instrumentation

Question 274

List the symptoms of acute bacterial prostatitis

Answer 274

* Fever * Perineal/back pain * UTI * Urinary retention * Diffuse oedema * Microabscesses

Question 275

What are the likely causative organisms in acute bacterial peritonitis?

Answer 275

* Gram negative bacilli, e.g. E.coli, Proteus sp. * S aureus (MSSA, MRSA) * N gonorrhoea (less common)

Question 276

What investigations should be done in acute bacterial prostatitis?

Answer 276

* Urine culture, usually positive * Blood culture * Trans-rectal U/S * CT/ MRI * Obtaining prostatic secretions NOT advisable

Question 277

What are the complications of acute bacterial prostatitis?

Answer 277

* Prostatic abscess * Spontaneous rupture * Urethra, rectum * Epididymitis * Pyelonephritis * Systemic sepsis

Question 278

Describe antibiotic management of acute bacterial prostatitis

Answer 278

* Check recent/previous microbiology * Ciprofloxacin/ofloxacin (no streptococcus cover) * D/W microbiology in systemic infections

Question 279

What causes chronic prostatitis?

Answer 279

* Rarely associated w/ acute prostatitis * May follow chlamydia urethritis * Recurrent UTIs

Question 280

List the symptoms of chronic prostatitis

Answer 280

* Most asymptomatic * Perineal discomfort/back pain * +/- low grade fever * UTI symptoms

Question 281

What are the common causative organisms in chronic prostatitis?

Answer 281

* Gram negative bacilli, e.g. E.coli, Proteus sp. * Enterococcus sp. * S aureus (MSAA, MRSA)

Question 282

What is epididymitis?

Answer 282

Inflammatory reaction of the epididymis Relatively common

Question 283

Describe the aetiology of epididymitis

Answer 283

* Ascending infection from urethra * Urethral instrumentation

Question 284

List the symptoms of epididimytis

Answer 284

* Pain, fever, swelling, penile discharge * Symptoms of UTI/urethritis

Question 285

List the common causative organisms of epididimytis

Answer 285

* GNB, enterococci, staphylococci * TB in high risk areas and individuals * In sexually active men * Rule out chlamydia and N gonorrhoea (urethritis)

Question 286

What is orchitis?

Answer 286

Inflammation of one or both testicles

Question 287

List the symptoms of orchitis

Answer 287

* Testicular pain and swelling * Dysuria * Fever * Penile discharge

Question 288

Describe the aetiology of orchitis

Answer 288

* Usually viral * Mumps * Bacterial

Question 289

What causes bacterial orchitis?

Answer 289

* Complication of epididimytis * Rule out sexually transmitted bacteria

Question 290

How does bacterial orchitis present?

Answer 290

Acutely unwell

Question 291

How is bacterial orchitis managed?

Answer 291

* IV antibiotics * As per complicated UTI * Urgent urological review

Question 292

What are the complications of bacterial orchitis?

Answer 292

* Testicular infarction * Abscess formation

Question 293

What is Fournier's gangrene?

Answer 293

* Form of necrotising fasciitis affecting the genitals/perineal area * Rapid onset and spreading infection * Systemic sepsis

Question 294

What age group are most often affected by Fournier's gangrene?

Answer 294

Usually \>50 y/o

Question 295

List the risk factors for Fournier's gangrene

Answer 295

* UTI * Complications of IBD * Trauma * Recent surgery

Question 296

What pathogens commonly cause Fournier's gangrene?

Answer 296

Mixed infections, mainly gram -ve bacteria and anaerobes

Question 297

What investigations should be done in Fournier's gangrene?

Answer 297

* Blood cultures * Urine * Tissue/pus - culture

Question 298

How is Fournier's gangrene managed?

Answer 298

* Surgical debridement 1st line * D/W microbiology * Broad spectrum/combination antibiotics initially * E.g. Pip-tazobactam + Gentamicin + Metronidazole +/- Clindamycin

Question 299

Describe the gross anatomy of the kidneys

Answer 299

* Paired retroperitoneal organs * Located T12-L3 * Right lower than L * Normally 10-12cm length, 5-7cm wide, 3cm thick * Gerota's fascia covers - deficient inferiorly * Upper pole more posterior + medial, medial surface more anterior

Question 300

Describe the anatomy of the ureters

Answer 300

* 25-30cm long, 4-5mm calibre * 3 segments * Proximal: PUJ-pelvic brim * Mid: segment over sacral bone * Distal: lower sacral border to UO * 4 layers – vary depending on site * Urothelial mucosa * Lamina propria * Muscular layer * Adventitial layer

Question 301

Where do the ureters narrow physiologically? Why is this clinically relevant?

Answer 301

* Physiological narrowing * Pelvic ureteric junction (PUJ) * Crossing iliac at pelvic brim * Vesico-ureteric junction (VUJ) * Where calculi likely to obstruct - may limit flexi-regid ureteroscopies

Question 302

Describe the prevalence of kidney stones

Answer 302

* 10% Caucasian men develop stone by 70 years * Prevalence increasing * Once a stone has formed 50% will form another within 10 years

Question 303

List the risk factors for kidney stones

Answer 303

* Intrinsic factors * Sex - M:F 2:1 (closing) * M - higher oxalate production, F - higher urinary citrate * Age - peak 20-50 years * Family history * Comorbid conditions * Extrinsic factors * Fluid intake - \<1200ml/day * Diet * Lifestyle - sedentary * Climate * Country of residence (USA highest - but we are catching up) * General high incidence in hot climates

Question 304

Describe the genetic risks for kidney stones

Answer 304

* Uncommon in Blacks * More common in Caucasian, Asian * 25% family history * Familial renal tubular acidosis * Cystinuria

Question 305

What kind of diet predisposes to kidney stones?

Answer 305

* High animal protein (high oxalate, low pH, low citrate) * High salt (hypercalciuria) * Low calcium diets

Question 306

Why is the composition of kidney stones clinically relevant?

Answer 306

* If presenting in emergency doesn't matter * Different types can be v hard or soft - may influence management * Most commonly calcium oxalate * If other type something more may need to be done e.g. cysteine likely to be genetic, urate can be managed w/ medication * ESWL unlikely to be successful for calcium oxalate dihydrate - v hard * Some types are radio-opaque and some aren't

Question 307

List the most common types of kidney stones by composition

Answer 307

* Calcium oxalte - 80-85% * Uric acid - 5-10% * Calcium phosphate and calcium oxalate - 10% * Pure calcium phosphate - rare * Struvite (infection stones), Mg, ammonium, phosphate - 2-20% * Cysteine - 1%

Question 308

Which kidney stones are radio-opaque?

Answer 308

* Calcium oxalate, calcium phosphate, calcium oxalate - radio-opaque * Struvite, cysteine - relatively radiolucent * Uric acid - radiolucent

Question 309

Why do calcium oxalate kidney stones form?

Answer 309

* Excess oxalate * Commonly found in some fruit, vegetables, nuts and chocolate

Question 310

What causes a struvite stone to form?

Answer 310

* Caused by infection of urinary tract * Can grow quickly and become quite large

Question 311

Why do uric acid stones form?

Answer 311

* Chronic dehydration * Risk increases in those with gout, a genetic tendency or a diet too high in protein

Question 312

Why do cysteine stones form?

Answer 312

* Genetic condition - cysturia * Causes kidneys to excrete an excess of certain amino acids e.g. cysteine

Question 313

Why do xanthine stones form?

Answer 313

* Enzyme deficiency - xanthine oxidase deficiency * Causes build up of xanthine deposits

Question 314

Why do silica stones form?

Answer 314

* Rare, caused by certain medications or herbal supplements

Question 315

How do kidney stones form?

Answer 315

* Under-saturated * Supersaturated but stable – metastable * Supersaturated with spontaneous precipitation – unstable * Saturation product – level at which no more solute will dissolve in a solution without change in pH, temp * Formation product – level at which spontaneous formation occurs

Question 316

List the factors that affect kidney stone formation

Answer 316

* Low volume * Low pH (acidic) * Low citrate * Low magnesium * High uric acid * High calcium * High oxalate

Question 317

How do kidney stones present?

Answer 317

* Incidental * Imaging for another reason * Pain * Colic, radiates from loin to groin, cannot settle, unable to stay still * Haematuria * Visible or non visible * Sepsis/infection * Unknown source until imaged

Question 318

What initial investigations should be done in kidney stones?

Answer 318

* History and examination * Bloods * U&E, CRP, FBC * Urine * Non visible haematuria = 85% * Imaging * Gold standard = CT KUB (non contrast)

Question 319

Describe the biochemical tests which should be done following a patients first kidney stone

Answer 319

* U&E * Calcium * Urate * Urine dip * MSSU * (Sodium nitroprusside – Cystine) * Stone analysis

Question 320

What biochemical tests should be done in recurrent kidney stones?

Answer 320

* U&Es * Calcium * Urate * Venous bicarbonate * 24 hour urine analysis

Question 321

Why is CT KUB the gold standard for kidney stone imaging?

Answer 321

* 94-100% sensitivity * 92-100% specificity * Other benefits * Stone diameter * Skin to stone distance * Hounsfield units * No contrast * Lower radiation dose

Question 322

How effective is ultrasound in imaging kidney stones?

Answer 322

* 45% sensitivity * 88-94% specificity

Question 323

How effective is X-ray KUB for imaging kidney stones?

Answer 323

* 44-77% sensitivity * 80-87% specificity * Better for follow up of known stone

Question 324

Describe the risk of radiation exposure in imaging

Answer 324

* Annual background radiation 2-3mSV * Annual occupational limit 50mSV * Lifetime risk of fatal cancer 20% * Radiation dose 10mSV increases risk by 0.05% (1in 2000) * CXR - 0.02 * XRAY KUB - 0.5 * CT KUB - 4.7

Question 325

How are kidney stones managed medically?

Answer 325

* Analgesia * NSAIDs or opiates? * NSAIDs reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis * Medical Expulsive Therapy * Lancet 2015 – multicentre, randomised, placebo controlled trial - no benefit from tamsulosin

Question 326

What are the surgical options for management of kidney stones?

Answer 326

* Various options depending on location and size * Ureteroscopy and basket * Ureteroscopy and fragmentation * FURS – flexible ureteroscopy * ESWL – extracorporeal shockwave lithotripsy * PCNL – percutaneous nephrolithotomy * Emergency stent or nephrostomy

Question 327

When is admission required in kidney stones?

Answer 327

* Uncontrollable pain * Fever or signs of sepsis * Solitary kidney with a ureteric stone * Bilateral ureteric stones * Renal failure caused by an obstructing stone * If discharging a patient be sure to give them clear worsening advice and when to come back to hospital

Question 328

Describe the emergency presentation of kidney stones with pain, what are the differential diagnoses for this pain?

Answer 328

* Worst pain ever * Worse than labour * Typical loin pain which radiates to groin * Beware in male it can be testicular or penile pain * BEWARE AAA * Other differentials * Appendicitis * Gyn pathology

Question 329

What do we worry about in an emergency presentation of kidney stones?

Answer 329

Infected obstructed systems: A patient with sepsis and obstructing stone is a urological emergency and must be seen and assessed urgently

Question 330

How should a patient with infected obstructed systems be managed?

Answer 330

* Take full history and examine the patient * Is there any evidence of sepsis? * Implement “sepsis 6” protocol * Cultures and antibiotics * Check bloods for renal function and inflammatory markers * Urgent imaging – USS or CT * The patient may need urgent decompression of an obstructed infected collecting system by nephrostomy or ureteric stenting

Question 331

Describe the sepsis 6

Answer 331

1. Give O2 to keep sats above 94% 2. Take blood cultures 3. Give IV antibiotics 4. Give a fluid challenge 5. Measure lactate 6. Measure urine output

Question 332

Describe the presentation of elective stones

Answer 332

* Pain * Recurrent urinary tract infections * Haematuria * Incidental finding on scan * AKI/CKD

Question 333

How can elective kidney stones be managed?

Answer 333

Various options depending on patient factors, patient choice, location and size, symptoms * Observation * Ureteroscopy and basket * Ureteroscopy and fragmentation * FURS – flexible ureteroscopy * ESWL – extracorporeal shockwave lithotripsy * PCNL – percutaneous nephrolithotomy * Emergency stent or nephrostomy

Question 334

What is ESWL? How is it used in the management of kidney stones?

Answer 334

* Produces a shockwave * Electrohydraulic * Electromagnetic * Piezoelectric * Direct effect * Shearing * Spalling * Cavitation effect * Shockwave in fluid causes a microbubble * Dissolved gas in fluid around bubble expands into bubble * Bubble collapses * Microjets * Pit stone surface

Question 335

What are staghorn calculi? How are they treated?

Answer 335

* Staghorn calculi refer to branched stones that fill all or part of the renal pelvis and branch into several or all of the calyces * They are most often composed of struvite (magnesium ammonium phosphate) * Percutaneous Nephrolithotomy (PCNL)

Question 336

How common are tumours of the urinary tract

Answer 336

* Prostate, kidney, bladder - 3 of top 8 cancers * Prostate and renal cancer on the rise * Prostate cancer is most common cancer death in men

Question 337

What is the prostate cancer iceberg?

Answer 337

* Symptomatic cases only a small proportion of the histological prevalence * Autopsy studies * Live long enough all will get - myth?

Question 338

Describe the epidemiology of prostate cancer

Answer 338

* Commonest urological malignancy * 2nd commonest cause of male cancer death * Cancer specific 10 year survival is 84%

Question 339

Describe the incidence of prostate cancer

Answer 339

* 1 in 6 UK males will be diagnosed with prostate cancer in their lifetime * 1 in 8 in 80 years probably over estimated, based on autopsy studies

Question 340

What are the risk factors for prostate cancer?

Answer 340

* Age - 85% diagnosed in over 65 y/o * Microscopic foci 30% 50 y/o and 70% \>80 y/o * Familial and genetic factors * 2x risk if 1st degree relative \<60 y/o * 4x risk if two 1st degree relatives (any age) * BRCA2 gene mutations reported * PTEN and TP53 - TSGs * Environmental/occupation * Industrial chemicals e.g. cadmium * Working in nuclear power industry or exposed to high levels of UV light * Hormones * Normal function regulated by testosterone and DHT * Men castrated before puberty/those deficient in 5 alpha reductase (converts T --\> DHT) almost never develop prostate cancer * Sexual behaviour - increased risk if sexually active at early age or history of STDs * Diet * Link between total fat consumption and prostate cancer deaths * High serum levels of alpha linolenic, palmitoleic and palmitic acid * Racial factors * African American 1.6x risk of white American * Geographic variations * Highest incidence in Westernised nations, least in Asia and Far East * US migrants from Japan and Asia 20x increase

Question 341

List the signs and symptoms of prostate cancer

Answer 341

* Local (66%) and locally advanced (27%) * OFTEN ASYMPTOMATIC * Painful or slow micturition, Urinary retention (may cause anuria, uraemia), Urinary tract infection * Haematuria - blood in urine * Lymphoedema * Metastatic (7%) * Bone pain - most common symptom of metastases * Renal failure- ureteric obstruction * Weight loss, lethargy Raised PSA level - on suspicion or screening

Question 342

List the methods of diagnosis/screening for prostate cancer

Answer 342

* DRE - digital rectal examination * PSA - prostate-specific antigen * PIRADS - Prostate MRI * TRUS - guided needle biopsy

Question 343

Describe the pathology of prostate cancer

Answer 343

* Adenocarcinoma * Usually arises in peripheral zone of prostate * Enlargement of prostate often due to BPH not cancer

Question 344

Describe the grading system for prostate cancer

Answer 344

Gleason grading stem - based on extent to which tumour cells are arranged into recognisable glandular structures, a spectrum of histological malignancies. Tumours given a score (Gleason Score) * Gleason score = sum of two most prominent Gleason grades seen histologically in a sample * \<4 - well differentiated, 25% 10-year likelihood of local progression * 5-7 - moderately differentiated, 50% 10-year likelihood of local progression * \>7 - poorly differentiated, 75% 10-year likelihood of local progression

Question 345

Describe the clinical use of prostate specific antigen

Answer 345

* Serine protease (33kD) secreted into seminal fluid * Responsible for liquefaction of seminal coagulation * Small proportion leaks into circulation * Tissue not Tumour specific * Great tumour marker * Poor diagnostic test * Tends to rise with age * Depends on prostate size * Other influences e.g. inflammation, infection

Question 346

How is PSA measurement used clinically?

Answer 346

* PSA measurements can provide information about prostate cancer from the initial screening and early detection through to the staging of the disease * Can also be used to monitor progression

Question 347

How is localised prostate cancer managed?

Answer 347

* Watchful waiting * Active Surveillance * Radiotherapy (with or without LHRH analogue) * External beam * Brachytherapy * Radical prostatectomy * Cryotherapy/HIFU * TURP if symptomatic

Question 348

Why aren't all patients with localised prostate cancer given treatment?

Answer 348

* Need life expectancy of 10 years to benefit from treatment for localised prostate cancer * Many will die of other causes before prostate cancer kills them

Question 349

Describe the metastatic complications of prostate cancer. How are they managed?

Answer 349

* Spinal cord compression * Urological emergency * Severe pain * Off legs * Retention * Constipation * Urgent MRI * Radiotherapy vs spinal decompression surgery * Ureteric obstruction * Anorexia, weight loss, raised creatinine * To nephrostomise or not and then to stent or not * Temporary measure will not improve cancer progression

Question 350

How is advanced prostate cancer treated?

Answer 350

* Androgen ablation therapy - medical castration (LHRH analogue) or surgical castration (orchidectomy) * Good response in 70-80%, long term outcome less favourable as remission not usually maintained * Lowers testosterone by 95% (testicular), adrenal remains * LHRH analogues have largely replaced surgical castration * Chemotherapy * TURP for relief of symptoms * Radiotherapy

Question 351

Describe the hypothalamic-pituitary-testicular axis

Answer 351

* LHRH secreted from hypothalamus, stimulates the pituitary to produce LH and FSH, stimulate the testes to secrete testosterone * ACTH released from pituitary gland after stimulation by CRH from hypothalamus, ACTH regulates secretion of adrenal androgens, some of which are converted to testosterone

Question 352

List the risk factors for bladder cancer

Answer 352

* Age – rare \<50yrs, most common 80th decade * Male \> Female * Race- more common in Caucasians * Chronic inflammation- stones, infection (schistosomiasis), long term catheters * Drugs - cyclophosphamide, pioglitazone * Pelvic radiotherapy * Occupation * Smoking - accounts for 30-50% of bladder cancers, risk only returns to normal after smoking cessation of 20 years

Question 353

Which drugs increase the risk of bladder cancer?

Answer 353

* Aromatic hydrocarbons - anilines * 25-45 year latency * 2-naphythlamine, 4-aminobiphenyl (4-ABP) * Liver metabolism but excreted in urine * E.g. pioglitazone, cyclophosphamide

Question 354

Describe the presentation of bladder cancer

Answer 354

* Classically painless frank haematuria * 25% serious cause for this in over 65s * All should have cystoscopy and upper tract imaging * Some present with microscopic haematuria (5% serious causes)

Question 355

Describe the pathology of bladder cancer

Answer 355

* Transitional cell carcinoma 90% * (Superficial 75% and invasive 25%) * Squamous carcinoma – 5% * Adenocarcinoma – 2% * Other secondaries

Question 356

Describe the staging of bladder cancer

Answer 356

* Carcinoma in situ * Ta - mucosa * T1 - into lamina propria * T2 - into inner muscle layer * T3a - into outer muscle layer * T3b - through outer muscle layer * T4a - into prostate gland * T4b - into bony pelvis Non-muscle invasive bladder cancer vs muscle invasive bladder cancer

Question 357

Describe the initial treatment of bladder cancer

Answer 357

* Diagnosed at flexible cystoscopy * Urgent TURBT (trans-urethral resection of bladder tumour) * CT IVU (5% chance upper tract involvement) * Bimanual examination carried out at TURBT

Question 358

How is localised bladder cancer treated?

Answer 358

* Cytoscopy and resection (TURBT) - to confirm presence of bladder cancer and see its location, number and extent * Non-muscle invasive * Tis - intravesical chemotherapy * Ta - intravesical chemotherapy or observation * T1 * Low grade - intravesical chemotherapy * High grade - cystectomy * Muscle invasive * T2a/T2b * For cystectomy candidates - cystectomy +/- chemotherapy * For non-cystectomy candidates - radiotherapy +/- chemotherapy

Question 359

What chemotherapy is used in bladder cancer?

Answer 359

* Mitomycin C * Once off or 6 week course * DNA synthesis

Question 360

Describe the immunotherapy used in bladder cancer

Answer 360

* Immunotherapy * Induction and maintenance * Cell mediated immune response

Question 361

How is a radical cystectomy carried out?

Answer 361

* Bladder and prostate/uterus removed * Urine diverted * Mortality 2% * Sometimes required after radiotherapy failure 'salvage cystectomy'

Question 362

List the most common types of renal cancer

Answer 362

* 85% renal cell carcinoma * Others * Transitional cell carcinoma * Sarcoma * Metastases

Question 363

Describe the epidemiology of renal cancer

Answer 363

* Age peak 40-70 y/o * Male \> females 2:1

Question 364

List the risk factors for renal cancer

Answer 364

* Smoking (RR 1.4-3.0) * Causes chronic hypoxia and DNA damage secondary to benzo (alpha) pyrene diolepoxide (BPDE) * Obesity (RR 1.5-3.0) * Hypertension * Acquired renal cystic disease (RR 4) * Haemodialysis * Genetics- VHL (vhl), HPRCC (Met), HLRCC (FH), Birt-Hogg-Dube (FLNC), Tuberous sclerosis (TS) * VHL 3p penetrance 1 in 36000 - phaeochromocytoma, renal and pancreatic cysts, RCC, cerebellar hemangioblastoma

Question 365

How does renal cancer present?

Answer 365

* 80% incidental * \<25% systemic symptoms- * Night sweats, fever, fatigue, weight loss * 10% classic triad- mass, pain, haematuria * Varicocele * Lower limb oedema * Paraneoplastic syndromes

Question 366

Which paraneoplastic syndromes could renal cancer present with?

Answer 366

* Polycythaemia (3-10%) * Hypercalcaemia (3-13%) - either from a PTH-like substance, or from osteolytic hypercalcaemia * Hypertension (up to 40%) renin secretion * Deranged LFT’s - Stauffer’s syndrome, from hepatotoxic tumour products * Rare: * ACTH (Cushing’s syndrome) * Enteroglucagon (protein enteropathy) * Prolactin (galactorrhoea) * Insulin (hypoglycaemia)

Question 367

How is renal cancer diagnosed?

Answer 367

* Initial diagnosis: * Usually on USS * CT kidneys +/- MRI RV * Renal Biopsy * CT Chest * Histology: * Conventional or clear cell (80%)- vascular, granular and clear (lipids) * Papillary (10%) * Chromophobe (5%)- large polygonal Collecting duct- rare Medullary cell- rare

Question 368

Describe the staging of renal cancer

Answer 368

* T1a \<4cm * T1b 4-7cm * T2 \>7cm * T3a into renal vein * T3b IVC below diaphragm * T3c IVC above diaphragm * T4 beyond Gerota’s and/or adrenal gland Perioperative mortality 3% in I, 9% in II/IV Downstaging of great surgical importance e.g. IV to III

Question 369

Describe the treatment of metastatic renal cancer

Answer 369

Tyrosine kinase inhibitors

Question 370

Describe the epidemiology of testicular cancer

Answer 370

* Most Common solid cancer in men 20-45 * Most curable cancer * Increasing Incidence

Question 371

List the risk factors for testicular cancer

Answer 371

* Age 20-45y/o * Cryptorchidism * HIV * Caucasian population

Question 372

What investigations should be done in testicular cancer?

Answer 372

* Scrotal ultrasound * Tumour markers: * Alpha-fetoprotein (50-70% Teratoms and Yolk Sac Tumours) * Beta hCG (40% Teratoma, 15% Seminoma) * LDH (10-20% Seminoma) * CT staging if advanced

Question 373

Describe the classification of testicular cancer

Answer 373

* Germ cell tumours (most common) * Seminoma * Teratoma * Mixed * Yolk sac * Stromal tumours (10% malignant) * Leydig * Sertioli * Other * Lymphoma * Metastasis

Question 374

How is testicular cancer treated?

Answer 374

* Radical Orchidectomy * Chemotherapy * Para-aortic nodal radiotherapy * Retroperitoneal Lymph Node Dissection

Question 375

Describe the prevalence of penile cancer

Answer 375

* Rare (0.2% male cancers in the west) * Associated with HPV infection (16,18,21); smoking * Premalignant lesions: chronic changes * Even rarer in males circumcised at birth

Question 376

How is penile cancer treated?

Answer 376

* Circumcision * Topical treatment CO2/5FU * Penectomy +/- reconstruction * Lymphadenectomy * Chemo-radiotherapy

Question 377

Where does a transplant kidney go?

Answer 377

* Old kidneys left in the body * Donor kidney usually placed in the groin and attached to blood vessels and the bladder * Ureter carries urine from new kidney to the bladder

Question 378

How is kidney failure defined? What are the options in kidney failure?

Answer 378

When your kidneys have failed (eGFR 7-10ml/min) what are your options? * Dialysis * Transplantation * Conservative care

Question 379

What do patients dislike most about dialysis?

Answer 379

* Always exhausted * Fluid restriction * Restricted diet - K+, PO4- * Women are infertile * Reduced life expectancy - I'm going to die soon

Question 380

What are the benefits of kidney transplant vs dialysis?

Answer 380

* Increase life expectancy * Increase quality of life * Less time in hospital etc.

Question 381

Which patients are unsuitable for kidney transplant?

Answer 381

* Reduced life expectancy * Older age * Co-morbidity * Unlikely to survive 5 yrs * Surgical contraindications * No bladder * Calcified BVs * Medical contraindications * Hypertension * Hypotension * Diseases that will recur in the transplant

Question 382

Which renal disease are treated in the dialysis clinic vs the transplant clinic?

Answer 382

* Dialysis clinic * Renovascular disease * T2 diabetic nephropathy * Vasculitis * Obstructive uropathy * Transplant clinic * APKD * Glomerulonephritis * Reflux nephropathy * T1 diabetic nephropathy

Question 383

Where do transplant kidneys come from?

Answer 383

* Deceased donors: * Brain stem death – heart beating/non-heart beating * No malignancy or unidentified/untreated infections * Good kidney function – you only get one kidney * Kidneys donated in any part of the UK are allocated to most appropriate patient in UK via NHS Blood & Transplant * Average waiting time 2-3 years * Around the world * Living donors: * Relative * Friend * Social media 'friend' - directed altruistic * Altruistic donor

Question 384

What are the advantages of living vs deceased kidney donation?

Answer 384

* Pre-emptive transplantation * Better kidneys * Better outcomes - longer kidney survival

Question 385

What are the requirements for living kidney donation?

Answer 385

* Donor * Fit and healthy * Excellent kidney function * Blood group and HLA compatible - or not

Question 386

Describe the financial indications for kidney transplant

Answer 386

* Average costs England 2003 (NHS commissioning board 2013) * Transplantation * £17,000 for first year * £5,000 for every subsequent year * Dialysis - £30,800

Question 387

What is the challenge with kidney transplant?

Answer 387

* Immune system * Recognised foreign cells and proteins * Responds to destroy foreign tissue through complex amplification pathways * Evolved to deal w/ infection and malignancy * Recognising cell surface proteins as ‘non-self’ * Blood group incompatibility * HLA incompatibility * T cell mediated and antibody mediated rejection

Question 388

Describe the pathogenesis of immune rejection in a kidney transplant

Answer 388

* Antigen presenting cell presents foriegn antigenic peptide from graft to T cell * Binds to T cell receptor and activates T cell * Cascade of events activating * T-helper cells * NK cells * Macrophages * B cells * Antibody production * = death of foriegn cell type

Question 389

How is graft rejection prevented in kidney transpants?

Answer 389

* Immunosuppression * Galiximab – chimeric mouse-human monoclonal antibody directed against IL-2 receptor * Tacrolimus – calcineurin inhibitor * Mycophenolate mofetil - inhibitor of inosine-5'-monophosphate dehydrogenase - depletes guanosine nucleotides in T and B lymphocytes and inhibits proliferation * +/- Steroids

Question 390

List the complications of kidney transplantation

Answer 390

1. Rejection 2. Infection 3. Malignancy

Question 391

Describe rejection in kidney transplantation

Answer 391

* Cell-mediated rejection – interstitial inflammation and tubulitis * Often easily treated with steroids if caught early * Antibody-mediated rejection – endothelial swelling, glomerulitis and peri-tubular capillaritis * Donor specific antibodies * Often difficult to treat Increase immunosuppression

Question 392

Describe infection in kidney transplant, how is it treated?

Answer 392

* Common organisms in common sites * Chest infection Skin/wound infections * Urine infection * Re-activation infections * CMV disease – pneumonitis, colitis, hepatitis, renal disease * BK nephropathy * Uncommon organisms * Pneumocystis jjrovecii * Reduce immunosuppression * Treat with antibiotic/anti-viral

Question 393

Describe malignancy in kidney transplantation, how is it treated?

Answer 393

* Kaposi sarcoma\* (KS; SIR 61 and EAR 15) * Skin (nonmelanoma, nonepithelial SIR 13.9 and EAR 22) * Non-Hodgkin lymphoma (SIR 7.5 and EAR 168) * Lung (SIR 2.0 and EAR 85) * Kidney\*\* (SIR 4.7 and EAR 76) * Colon and rectum (SIR 1.2 and EAR 15.8) * Pancreas (SIR 1.5 and EAR 6.4) * Hodgkin lymphoma (SIR 3.6 and EAR 7.9) * Melanoma (SIR 2.4 and EAR 29) Reduce immunosuppression +/- rituximab or chemotherapy

Question 394

Describe the fluid compartments of the body

Answer 394

* 2/3 of body weight fluid * 2/3 intracellular - harder to access * Potassium * 1/3 extracellular - more prone to fluctuation * Interstitium (30%) - sodium chloride * Plasma (7%)

Question 395

Describe the fluid distribution of a 75kg person

Answer 395

* Intravascular 5L * Interstitial 10L * Intracellular 30L

Question 396

Describe the normal fluid intake and output

Answer 396

* Normal intake * 20-30ml/kg/day water * If 75kg = 2L/day * 50kg = 1.5L/day * Normal output * Total losses approx. 2L/day * Urine losses 500-1500 mls/day * Insensible losses 500mls/day

Question 397

Describe the fluid input and output of a 70kg male

Answer 397

* Input * Drinking - 1.5L * Food - 0.5L * Metabolic - 0.5L * Total = 2.5L * Output * Urine - 1.5L * Respiration - 0.4L * Sweating - 0.5L * Faeces - 0.1L * Total = 2.5L

Question 398

What can go wrong w/ fluid/electrolyte balance?

Answer 398

* Imbalance between input and output/losses * Not able to eat or drink - drowsy/fasting/obstruction * Medicine - laxatives, diuretics * Excess losses - diarrhoea, vomiting, polyureic (e.g. diabetes insipidis), pyrexical * Redistribution of fluid * Osmolar problems

Question 399

How can imbalance between input and output of water occur?

Answer 399

* Altered input * Inadequate hydration * Overhydration * Altered output * Excess losses * Vomiting * Diarrhoea * Stoma * Drains * Fever * Polyuria * Poor output * Oliguria

Question 400

Describe the electrolyte content of body fluids

Answer 400

* Gastric * High chloride content - vomiting can result in hypochloraemia * Diarrhoea * High potassium content - can result in hypokalaemia

Question 401

What can cause redistribution of fluids?

Answer 401

* Nephrotic syndrome * Patient hypoalbuminaemic - osmotic pressure in plasma lost, fluid into interstitium (extracellular or 3rd space)

Question 402

Describe the normal osmolarity of serum

Answer 402

* Normal serum osmolarity is 280-300 mOsm/kg * This is a measure of the serum concentration of small diffusible ions, mainly Na, K, glucose and urea (sodium is most important) * Together these ions exert a ‘pressure’ which causes water to move across cell membranes from weaker to stronger solutions until the concentration of solutes is equal on both sides

Question 403

What is the clinical relevance of the osmolarity of body fluids?

Answer 403

* Risk of cerebral oedema i.e. water from ECF --\> ICF * In acute hyponatraemia or out of brain if sodium corrected too quickly

Question 404

What are the aims of fluid management?

Answer 404

* Oral route is always best if possible - patient's drink to thirst and fluid balance achieved naturally * If oral not available IV fluids What are the aims of fluid management? * Maintenance –water and electrolytes * Daily fluid requirements + insensible loss * Replacement * To replace ongoing losses (vomit, diarrhoea, fistulae, stoma output etc.) * Resuscitation * To correct an intravascular or extracellular volume deficit

Question 405

What 5 questions should be asked before prescribing fluid?

Answer 405

1. Is the patient dry, wet or euvolaemic? 2. Does the patient need IV fluid? 3. Why does the patient need IV fluid? 4. How much fluid? 5. What type of fluid?

Question 406

How can you assess volume status?

Answer 406

* Fluid depletion * Relevant history - abnormal losses? Diuretic therapy? * Symptoms - thirst, dry mouth, dry skin, dark urine, postural dizziness * Signs - reduced skin turgor, dry mouth, dry axillae, CRT \>2 secs, postural hypotension, tachycardia, tachypnoea * Laboratory tests - UEs (esp high urea) * Monitoring - BP + heart rate, response to fluid challenge, urine output, fluid balance, daily weight, CVP * Fluid overload * Relevant history - heart failure? Renal failure? * Symptoms - breathlessness, swollen ankles * Signs - hypertension, increased JVP, 3rd heart sound, pulmonary/peripheral oedema * Laboratory tests - serum albumin

Question 407

What are the NICE guidelines 5 R's for fluid management?

Answer 407

* Resuscitation * Routine maintenance * Replacement * Redistribution * Reassessment

Question 408

List the types of IV fluid

Answer 408

* Crystalloids * Saline (various, 0.9% is standard) * Dextrose (various, 5% is standard) * “Balanced solutions” (eg Hartmann’s or Ringer’s lactate) * (Sodium bicarbonate (1.26%) – expert advice only) * Colloids * E.g. Gelofusion or starch-based fluid * Larger molecules - stay intravascular and restore circulation but studies show poorer outcomes, not used frequently * Blood products * Packed red cells * Platelets or fresh frozen plasma (clotting factors) * Human albumin solution

Question 409

Where does IV colloids, saline/Hartmann's and Dextrose go?

Answer 409

* Collid - stay intravascular * Saline/Hartmann's - equilibriate between intravascular and interstitial compartments * Dextrose like giving water - moves intracellularly, not good for resuscitation (lost from interstitium and intravascular space)

Question 410

When is sodium bicarbonate used?

Answer 410

In renal failure

Question 411

What are the clinical signs of hypovalaemia ('shock')?

Answer 411

* Hypotension (systolic BP \<100 mmHg) * Tachycardia (HR \>90 bpm) * Peripherally cool * Capillary refill time \>2 secs * NEWS \>5 * Passive leg raising suggests fluid responsiveness

Question 412

Which IV fluids are used for resuscitation?

Answer 412

Fluid bolus, usually saline or Hartmann's - stay extracellular

Question 413

How can the amount of fluid needed for routine maintenance be calculated?

Answer 413

* Calculate requirements based on * Projected losses * Any intake e.g. IV drug volumes/NG feed

Question 414

When should you ask for seniour help when prescribing fluid for replacement/redistribution?

Answer 414

* Any time you aren’t sure what to do. * Specific situations with complex fluid and electrolyte redistribution issues: * Gross oedema * Severe sepsis * Peripherally vasodilated - no amount of fluid will correct BP * Hyponatraemia/hypernatraemia - care not to correct too quickly * Renal, liver and/or cardiac impairment * Post-operative fluid retention and redistribution * Malnourishment/feeding issues

Question 415

Describe reassessment in fluid management

Answer 415

* Daily UEs and fluid balance * Remember IV drugs contribute * Consider daily bicarbonate/magnesium if abnormal GI or renal losses * Review need for IV fluid daily, and adjust rate appropriately * Inappropriate IV fluid = IV access for prolonged time (risk of infection), fluid overload and electrolyte imbalances