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Phase 3 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Describe the structure of the glomerular filtration barrier

A

Constriction of afferent arteriole is controlled by SNS

Constriction of efferent arteriole is controlled by angiotensin II

Layers of filtration

Fenestrated capillary endothelium (endothelial cells covered by glycocalyx)

Negatively charged glomerular basement membrane

Foot processes of podocytes
> Wrap around capillaries and leave slits between them for blood to filter through

> Podocytes secrete the basement membrane

> . Filtration slits (slit diaphragm)

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2
Q

Describe how urea is processed and how its levels may change

A

Byproduct of amino acid metabolism in liver

Reabsorbed in inner medullary collecting ducts (passively)

Changes in urea

Diet
> High protein or GI bleed leads to high urea

Tissue breakdown e.g. corticosteroid
> High urea

Liver failure
> Lowers urea

Dehydration
> Passive reabsorption in proximal tubule - high urea

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3
Q

Explain why creatinine is used to measure renal function

A

Normal product of muscle metabolism

Provides good estimate of GFR because
> Daily production is constant
> (almost) fully filtered at the glomerulus
> Neither reabsorbed nor secreted (almost) in the tubule

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4
Q

Describe the limitations of eGFR

A

Only accurate in steady state and assumes average muscle mass
> Overestimation of function those with lower muscle mass e.g. amputees, para/quadriplegics, rheumatoid arthritis

eGFR not accurate >60ml/min and <18 years of age

Inverse relationship between GFR and serum creatinine leads to
> Slow recognition of loss of the first 70% of kidney function
> Surprise at the sudden rise in creatinine

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5
Q

Desribe the formulae used to calculate eGFR

A

Cockgroft and Gault formula for estimating creatinine clearance
> Attempts to correct for muscle mass

MDRD 4-variable formula for estimated GFR
> Based on serum creatinine, age, sex

eGFR < 60ml/min/1.73m2 or raised serum creatinine means reduced kidney function (adults)

CKD-EPI equation for patients with high levels of eGFR

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6
Q

Describe acute interstitial nephritis

A

May have raised eosinophil count and rash

  • Haematuria, fever, oliguria
  • Swelling, nausea, vomiting

Caused by autoimmune disorders, systemic disorders, infections, allergic reaction to antibiotics, anticonvulsants, diuretics…

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7
Q

Describe the staging of CKD

A

Stage 1:
Normal
GFR >90ml/min

Stage 2:
Early CKD
GFR 60-89ml/min

Stage 3:
Moderate CKD
GFR 30-59ml/min

Stage 4:
Severe CKD
GFR 15-29ml/min

Stage 5:
End-stage renal disease
GFR <15ml/min

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8
Q

Describe the measurement of urinary protein excretion

A

24h urine collection (g/24h)

Protein:creatinine ratio (PCR) on morning spot sample (mg/mmol)

Albumin:creatinine ratio (mg/mmol)

If excess proteinuria, the balance changes

30% other proteins
> Immunoglobulin
> Tamm Horsfall

70% albumin

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9
Q

Which cells and pathophysiological mechanisms are involved in glomerulonephritis?

A

Cells
- Parietal epithelial cells
- Podocytes
- Mesangial cells
- Endothelial cells
- Basement membrane

Pathophysiological mechanisms
- Antibodies, immune complexes, complement
- Cell-mediated mechanisms: cytokines, growth factors, proteinuria
- Metabolic / genetic / vascular causes

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10
Q

Describe the spectrum of presentations of glomerulonephritis

A

Incidental finding of urinary abnormalities +/- impaired kidney function

Visible haematuria

Synpharyngitic – sore throat and visible haematuria

Nephritic syndrome

Nephrotic syndrome

Acutely unwell with rapidly progressive glomerulonephritis

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11
Q

Describe nephrotic syndrome

A

Cause
> Damage to podocytes
> Scarring and deposits

Triad
> 3.5g proteinuria per 24h (urine PCR >300)
> Serum albumin <30
> Oedema

> (hyperlipidaemia)

Complications
> Venous thromboembolism
> Infection

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12
Q

Describe nephritic syndrome

A

More acute and inflammatory than nephrotic syndrome

Triad
> Hypertension
> Blood and protein in urine
> Declining kidney function (oliguria)

Berger’s disease (IgA nephropathy) is the most common cause of nephritic syndrome

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13
Q

Describe IgA nephropathy

A

Most common primary glomerular disease
> Precipitated by infection, can be synpharingitic
> May be secondary to HSP, cirrhosis, coeliac disease

Pathophysiology
> Abnormal overproduction of IgA1, IgA I/C
> Mesangial IgA, C3 deposition
> Mesangial proliferation

Clinical signs
> Haematuria
> Hypertension
> Proteinuria (varies with prognosis)

Complications
> End-stage renal failure (ESRF)

Treatment
> No specific therapy
> Antihypertensives
> ACE inhibitors
> SGLT2 inhibitors

Spectrum of disease
> Minor urinary abnormalities
> Hypertension
> Renal impairment and heavy proteinuria
> Rapidly progressive glomerulonephritis

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14
Q

Describe membranous glomerulonephritis

A

Presents with nephrotic syndrome
> Commonest primary cause
> Often chronic

Anti-phospholipase A2 receptor antibody – found in podocytes

IC in basement membrane / sub-epithelial space

Secondary causes
> Malignancy
> Connective tissue disease (CTD)
> Drugs

Variable natural history
> 1/3 spontaneously remit
> 1/3 progress to ESRF over 1-2 years
> 1/3 persistent proteinuria, maintain GFR

Treatment
> Treat underlying cause if secondary

> Supportive non-immunological
> ACEi
> Statin
> Diuretics
> Salt restriction

Specific immunotherapy
> Steroids
> Alkylating agents – cyclophosphamide

Alternative agents
> Rituximab: anti-CD20 MAb
> Cyclosporin
> Tacrolimus

Outcomes
> Complete or partial remission
> ESRD
> Relapse
> Death

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15
Q

Describe minimal change disease

A

Commonest form of glomerulonephritis in children
> 90% of GN <10 years, 20% of adults of all ages

Causes nephrotic syndrome

EM – foot process fusion

Causes
> Idiopathic
> Secondary to malignancy

Pathogenesis
> T cell and cytokine mediated
> Target podocytes, alter glomerular basement membrane charge

Clinical features
> Acute presentation
> May follow URTI
> GFR is normal or reduced due to intravascular depletion
> Rarely causes renal failure
> Not usually biopsied in children

Relapsing course – 50% will relapse

Treatment
> High dose steroids
> Prednisolone 1mg/kg for up to 8 weeks

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16
Q

Describe crescentic disease

A

Aka rapidly progressive GN

Group of conditions which demonstrate glomerular crescents on kidney biopsy

Nephritic presentation

Kidney biopsy
> Crescent-shaped collection of fibrin and matrix in Bowman’s space
> Can break through into surrounding cortex

Course of disease
> Aggressive disease – progress to ESRF quickly

Causes
> ANCA vasculitis – MPO/PR3
> Goodpasture’s syndrome: anti-GBM
> Lupus nephritis
> Infection-associated
> HSP nephritis

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17
Q

Describe diabetic nephropathy

A

Glomerulus
> Kimmelstiel Wilson lesions - nodules characteristic of DM
> Thickened basement membrane
> Associated with proteinuria

Pathophysiology
> Hyperglycaemia
> Volume expansion
> Intra-glomerular hypertension
> Hyperfiltration
> Proteinuria
> Hypertension and renal failure

Natural course
> After 20 years of diabetes
> Associated with other complications such as retinopathy
> Always with proteinuria
» Microalbuminuria
» Proteinuria
» Rise in serum creatinine

Management
> Treat hypertension
» ACEi or ARB
» Low sodium diet
» Weight loss
» Exercise

> Improve blood glucose control
> Education – DAFNE course
> Drugs
» Insulin
» Oral hypoglycaemia drugs including SGLT2 inhibitors
>Technology
» Glucose sensors and pumps

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18
Q

Describe renal artery stenosis

A

Clinical diagnosis
> No angiogram/CT angiogram/ MRI

Angioplasty/stenting is rarely effective

Pathophysiology
> Progressive narrowing of renal arteries with atheroma
> Perfusion falls by 20%

> GFR falls but tissue oxygenation of cortex and medulla maintained

> RA stenosis

> Cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways

> Parenchymal inflammation and fibrosis progresses and becomes irreversible

> Restoration of blood flow provides no benefit

Management
> Medical
» BP control (avoid ACEi and ARBs)
» 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

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19
Q

Describe amyloidosis

A

Deposition of highly stable insoluble proteinous material (amyloid) in extracellular space (felt-like substance made of beta pleated sheets)

Amyloid deposits in liver, heart, kidneys, gut

8-10mm fibrils sticking to wall

Test – Congo Red stain

Apple green birefringence – pathognomic

Electron microscopy
> Amyloid fibrils 9-11nm cause mesangial expansion

AA amyloid
> Inflammatory diseases e.g. chronic pyogenic or granulomatous infections, familial mediterranean fever (FMF)
> Causes systemic amyloidosis

AL amyloid
> Immunological fragments from haematological condition e.g. myeloma

Treatment
> AA amyloid
» Optimise treatment for underlying condition

> AL amyloid
> Optimise treatment for underlying condition

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20
Q

Describe lupus nephritis

A

Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease

> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)

> Auto-antibodies attach to basement membrane

> Activate complement (consumes C4)

> Renal damage

Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin

Kidney biopsy

Confirm diagnosis and stage disease

Poor prognosis

Treatment

Treat underlying disease

Immunosuppression

Steroids

MMF

Rituximab

Cyclophosphamide

Hydroxychloroquine

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21
Q

Describe lupus nephritis

A

Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease

> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)

> Auto-antibodies attach to basement membrane

> Activate complement (consumes C4)

> Renal damage

Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin

Kidney biopsy
> Confirm diagnosis and stage disease
> Poor prognosis

Treatment
> Treat underlying disease

> Immunosuppression
> Steroids
> MMF
> Rituximab
> Cyclophosphamide
> Hydroxychloroquine

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22
Q

Describe myeloma renal disease

A

Cast nephropathy

Hypercalcaemia / dehydration

Amyloid

Light chain deposition disease

Acquired Fanconi syndrome (proximal tubule dysfunction)

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23
Q

Describe the inheritance and clinical presentation of Adult Polycystic Kidney Disease (ADPKD)

A

Autosomal dominant pattern of inheritance

PKD 1 gene mutation in chromosome 16
> More common and aggressive, reach ESRF before 50
> Codes for polycystin 1

PKD2 gene mutation in chromosome 4
> Less common, less aggressive, may never reach ESRF)
> Code for polycystin 2

Clinical presentation
> Incidental finding on USS
> Hypertension
> Impaired renal function
> Loin pain
> Haematuria

Cysts gradually enlarge, normal kidney tissue replaced

Kidney volumes increased and eGFR falls

Complications
> Cyst infection, cyst rupture, haematuria and pain

Extra-renal manifestations
> Intra-cranial aneurysms
> Hypertension, LVH, valve abnormalities e.g. mitral valve prolapse
> Liver cysts
> Bronchiectasis
> Diverticular disease and abdominal hernias (due to size and pressure effect of enlarged kidneys)

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24
Q

Describe the function of polycystins

A

Polycystins are located in renal tubular epithelia & liver and pancreas ducts

Overexpressed in cyst cells

Membrane proteins involved in intracellular calcium regulation

Mechanism of cyst formation poorly understood

Genetic testing not routine but increasing

Vasopressin drives cyst development

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25
Q

Describe the diagnosis and management of ADPKD

A

Diagnosis

  • Family history
    > 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
  • Ultrasound
    > Differentiate between simple renal cysts
  • CT or MRI more sensitive
  • Genetic testing

Management
> Supportive
> Early detection and management of blood pressure
> Treat complications
> Manage extra-renal associations
> Prepare for renal replacement therapy

Tolvaptan
> Vasopressor antagonist, acts at V2 receptor - counteracts vasopressin
> Delays onset of RRT by 4-5 years
> Side-effects: hepatotoxicity, hypernatraemia

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26
Q

Describe Alport’s syndrome

A

Inherited progressive glomerular disease

Second most common inherited kidney disease

Caused by an inherited defect in type IV collagen (basement membrane) - found in ears, eyes and kidney

Usually X-linked - more severe presentation in males

Collagen IV abnormalities
> Alpha 3 gene mutation
> Alpha 4 gene (COL3A4) mutation
> Alpha 5 (COL3A5) mutation

Deafness and renal failure – can affect other organs including eyes

Presentation
> Asymptomatic persistent non-visible haematuria from early childhood

> Proteinuria, hypertension and progressive renal impairment

> ESRD – 90% on dialysis or transplanted by age 40

> Sensorineural hearing loss in late childhood

> Ocular defects
> Lens – anterior lenticonus
> Retina – bilateral white or yellow granulations
> Cornea – posterior polymorphous dystrophy, recurrent corneal erosion

Management
> Supportive – BP control
> Prepare for dialysis or transplant

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27
Q

Describe Fabry disease

A

Rare X-linked lysosomal storage disorder

Alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)

Also causes neuropathy, cardiac and skin features

GB3 accumulates in glomeruli, particularly in podocytes causing proteinuria and ESRF
> Pro-inflammatory and pro-fibrotic

Clinical presentation
> Intermittent episodes of burning pain in extremities
> Cutaneous vascular lesions – angiokeratomas
> Diminished perspiration
> Characteristic corneal and lenticular opacities
> Abdominal pain, nausea and/or diarrhoea
> Left ventricular hypertrophy
> Arrythmia
> Stroke
> CKD and proteinuria

Diagnosis
> Measure alpha-Gal A activity in leukocytes (unreliable in females)

> Renal biopsy
> Inclusion bodies of G3b aka zebra bodies

Management
> Enzyme replacement therapy; prevents progression to irreversible tissue damage

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28
Q

Describe the embryological development of the kidney

A

Pronephros

Mesonephros

Metanephros

Nephrogenesis commences in week 10

No new nephrons after 36 weeks

Approximately 1 million nephrons per kidney

GFR
> 120mls/min/1.73m2
> At birth: 40-65 mls/min/1.73m2

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29
Q

Describe the embryological development of the kidney

A

Pronephros

Mesonephros

Metanephros

Nephrogenesis commences in week 10

No new nephrons after 36 weeks

Approximately 1 million nephrons per kidney

GFR
> 120mls/min/1.73m2
> At birth: 40-65 mls/min/1.73m2

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30
Q

Describe renal hypodysplasia

A

Renal hypoplasia – reduction in number of nephrons but normal architecture

Renal dysplasia – malformed renal tissue

Renal hypodysplasia – congenital small kidneys with dysplastic features

Presentation

> Antenatal:US growth

> Neonate:
> Lung issues
> IUGR
> Acidosis
> Raised creatinine

> Children
> FTT
> Anorexia
> Vomiting
> Proteinuria

Management - supportive

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31
Q

Describe renal agenesis

A

Congenital absence of renal parenchymal tissue: metanephric stage

Male:female preponderance

Unilateral or bilateral (mostly sporadic)

Associated with increased risk of other anomalies

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32
Q

List renal cystic diseases

A
  • Multicystic dysplastic kidney (MCDK)
  • ADPKD
  • ARPKD
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33
Q

Describe multicystic dysplastic kidney (MCDK)

A

Abdominal mass detected antenatally or neonatally

Involution: 35-65%

Risks
> Hypertension
> Malignancy

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34
Q

Which anomaly is associated with ARPKD?

A

Congenital hepatic fibrosis: subclinical to liver disease

> Portal hypertension

> Ascending cholangitis

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35
Q

Describe the childhood presentation of ADPKD and its associated anomalies

A

Presentation
> Haematuria
> Hypertension
> Flank pain
> UTIs

Associated anomalies
> Mitral valve prolapse
> Cerebral aneurysm
> AVM
> Hepatic / pancreatic cysts
> Colonic diverticula / hernia

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36
Q

Describe hydronephrosis and list its causes in children

A

Male preponderance

Bilateral in some cases

Associated with renal injury and renal impairment

Postnatal US – renal pelvic diameter >10mm

Causes

> Vesico-ureteric reflux

> Obstruction of urinary tract

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37
Q

Describe vesico-ureteric reflux

A
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38
Q

Describe obstruction of the urinary tract in children

A

Level of obstruction

  • Pelvis/ureter (PUJ)
    > Partial/total blockage of urine at ureter junction with kidney

> Males > females
Bilateral in some

> Antenatal diagnosis
> Abdominal mass, UTI, failure to thrive (FTT)
> Abdominal or flank pain
> Ureter

  • Ureter/bladder (VUJ)
    > Vesico-ureteric junction obstruction

> Functional or anatomical abnormality

> > Megaureter
> Primary: reflux / obstruction
> Secondary: bladder issues

> > Ureteric dilation >7mm

  • Bladder
    > Posterior urethral valves
    » Most common obstructive uropathy
    » Antenatal detection
    » Investigations: US, MCUG
    » Bilateral hydronephrosis; UTI
    » Management – cystoscopy, ablation of valve
    » Risk of CKD and bladder dysfunction
  • Urethra
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39
Q

Describe the staging of AKI

A

Decline of renal excretory function over hours or days
> Avoid eGFR – not reliable in AKI
> Serum creatinine more reliable

Severity of AKI – KDIGO
- Stage 1
> Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline

  • Stage 2
    > Serum creatinine >2.0 and <3x AKI baseline
  • Stage 3
    > Serum creatinine 3x AKI baseline or
    > >354 micromol/l increase above AKI baseline

Oliguria
<1mL/kg/h in infants
<0.5mL/kg/h in children
<400-500mL/24h in adults

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40
Q

Describe the classification of the causes of AKI

A

Pre-renal
> Hypovolaemia + hypotension
> Reduced effective circulating volume
> Drugs
> Renal artery stenosis

Renal
> Glomerular
» Glomerulonephritis

> Tubular
> Ischaemic ATN
> Nephrotoxic ATN
> Myeloma cast nephropathy

> Tubulointerstitial
> Drugs
> Myeloma
> Sarcoid

Post-renal
> Renal papillary necrosis
> Kidney stones
> Retroperitoneal fibrosis
> Carcinoma of the cervix
> Prostatic hypertrophy/malignancy
> Urethral strictures

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41
Q

Describe the pre-renal causes of AKI

A

Hypotension

Hypovolaemia
> Blood loss
> Diarrhoea/vomiting
> Burns

Reduced effective circulating volume - hypoperfusion
> Cardiac failure
> Septic shock
> Cirrhosis

Hypoxia

Drugs
> ACEi
> NSAIDs

Toxins

Renal artery stenosis

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42
Q

Describe the renal causes of AKI

A

Large blood vessels
> Polyarthritis nodosa

Glomeruli and small blood vessels
> Glomerulonephritis
> Vasculitis

Tubular

> Ischaemic acute tubular necrosis (ATN)

> > Unresolved pre-renal causes:
> hypoperfusion or direct toxicity
> Hypotension
> Sepsis

Toxins

Exogenous
> Drugs
> NSAIDS, gentamicin, ACEi
> Contrast
> Poisons (metals, antifreeze)

Endogenous
> Myoglobin (rhabdomyolysis)
> Haemoglobin
> Immunoglobulins (myeloma)
> Calcium
> Urate

Nephrotoxic ATN
> Toxins (ethylene glycol, lithium), contrast, gentamicin
> Myeloma cast nephropathy

Tubulointerstitial
> Acute tubulointerstitial nephritis
> Rhabdomyolysis
> Drugs
> Myeloma
> Sarcoid

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43
Q

Describe post-renal causes of AKI

A
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44
Q

Describe glomerular haemodynamic regulation

A

Hypovolaemia leads to a fall in glomerular filtration pressure

Prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80 mmHg
> Blocked by NSAIDs

Efferent arteriole can vasoconstrict, increasing glomerular pressure
> Blocked by ACEi

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45
Q

Describe the investigations used in AKI

A

Acute or chronic

Bloods – both urea and creatinine elevated

Potassium must be controlled as it can cause heart problems

> <6.0 is abnormal but no immediate concern
6.0-6.4 risk of arrhythmia
>6.5 is a medical emergency

Urine output

Clinical assessment of fluid status
> BP, JVP, oedema, heart sounds

Underlying diagnosis – history, exam, meds

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46
Q

Briefly summarise the treatment of AKI

A
  • Circulation - restore renal perfusion
  • Treat hyperkalaemia
  • Treat pulmonary oedema if present
  • Remove causes: drugs, sepsis…
  • Exclude obstruction and consider renal causes
  • Refer to ICU or renal unit
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47
Q

Describe the treatment of hyperkalaemia

A

Protect the heart
> IV calcium gluconate 10ml 10% as cardiac membrane stabiliser

Drive K+ into cells
> Insulin 10-15 units actrapid + 50ml dextrose – moves potassium into cells

> If raised potassium and low bicarb, supplementation of bicarb – IV NaBicarb 1.26%

> Beta agonists – nebulised salbutamol

Remove K+ from body

> Acute

> > Haemodialysis
> Refractory potassium >6.5 mmol/l
> Refractory pulmonary oedema
> May be considered for
» Acidosis (pH < 7.1)
» Uraemia (pericarditis, encephalopathy)
» Toxins (lithium, ethylene glycol…)

> > Loop diuretic - furosemide

> Long-term
> Reduce absorption from gut – calcium resonium 15g/day orally or enema

48
Q

Describe the recovery from ATN

A

Polyuric phase 48-72h

Up to 6L urine/day

Often subsequent low K, Ca, Mg

Tubules fail to concentrate urine

49
Q

Define CKD and list causes

A

Kidney damage or GFR <60ml/min per 1.73m2 for 3 months or more

Aetiology
- Diabetic nephropathy
- Glomerular sclerosis
- Nodular lesions
- Proteinuria and deterioration of renal function
- Renovascular disease / ischaemic nephropathy
- Chronic glomerulonephritis
- Membranous glomerulonephritis
- IgA nephropathy
- Reflux nephropathy / chronic pyelonephritis
- ADPKD
- Obstructive uropathy

50
Q

Describe symptoms of CKD

A
  • Pruritus
  • Nausea, anorexia, weight loss
  • Fatigue
  • Leg swelling
  • Breathlessness
  • Nocturia
  • Joint/bone pain
  • Confusion

Advanced CKD
- Peripheral and pulmonary oedema
- Pericardial rub
- Rash/excoriation
- Hypertension
- Tachypnoea
- Cachexia
- Pallor & lemon yellow tinge

51
Q

Describe the treatment for anaemia as a consequence of renal failure

A

eGFR <30

Iron absorption and utilisation are suboptimal

Replace iron, B12 and folate if low

Treatment
> ESA (erythropoiesis stimulating agent) e.g. darbepoietin alfa 30 micrograms every 2 weeks

> Trigger usually Hb < 100g/L

> Target Hb is 100-120g/L

52
Q

Describe the pathophysiology and treatment of secondary hyperparathyroidism due to renal failure

A

Reduced 1-alpha hydroxylation of 25-hydroxycholecalciferol - low vitamin D, low calcium

Reduced phosphate excretion - high phosphate

High PTH – can lead to osteitis fibrosa cystica, left ventricular hypertrophy…

Treatment
> Activated vitamin D: alfacalcidol
> Mg supplements
> Phosphate binders
> Calcium-based: calcium carbonate/acetate
> Non-calcium: sevelamer, lanthanum, aluminium
> Calcimimetic: cinacalcet
> Parathyroidectomy

53
Q

Describe the management of CKD

A

Slowing progression

> Aggressive BP control - ACEi/ARB
Good diabetic control
Diet
Smoking cessation
Lowering cholesterol
Treating acidosis

Renal replacement therapy (RRT)

> Conservative care

> Home-based therapies

> > Home haemodialysis

> > > Most start with eGFR 6-8ml/min

> > > Side-effects
> Weight loss and persistent nausea
> Persistent hyperkalaemia
> Acidosis
> Severe hyperphosphataemia
> Pruritus
> Problematic fluid overload

> > Peritoneal dialysis

> Hospital-based therapies
> Hospital haemodialysis
> Self-care unit

> Transplant

54
Q

List the indications for renal replacement therapy

A

Medically resistant hyperkalaemia

Medically resistant pulmonary oedema

Medically resistant acidosis

Uraemic pericarditis

Uraemic encephalopathy

55
Q

List the symptoms a clinically uraemic patient would experience

A

Anorexia

Vomiting

Itch

Restless legs

Weight loss

Metallic taste

56
Q

Describe the mechanisms behind haemodialysis

A

> Hospital or home
Daily or nocturnal

Mechanism
> Blood is removed using a blood pump
> Passed through arterial circuit into dialysis filter
> Blood flows countercurrent to dialysis fluid
> Dialysis fluid is lower in concentration of solutes such as potassium, phosphate…
> Removal of solutes from blood e.g. potassium, urea occurs via diffusion down a concentration gradient
> Removal of fluid or “ultrafiltration” occurs through hydrostatic filtration
> Filtration removes fluid and dialysate is discarded
> Passes through dialysis filter into an air detector and back into patient
> Continuous loop for 4 hours

Access

> AVF access
> Arteriovenous fistula – connection between artery and vein

If veins not suitable for procedure, graft can be used

> TCVC (tunneled central venous catheter)

57
Q

Describe peritoneal dialysis

A

CAPD (continuous ambulatory peritoneal dialysis) or APD (automated peritoneal dialysis)

Daily or nocturnal

58
Q

Describe the process of kidney transplantation

A

Donor kidney placed in right or left iliac fossa

Ureter is shorter

Stent placed from donor kidney to bladder, removed a few weeks after transplantation

Native kidneys are left in body unless causing infection

59
Q

List the disadvantages of dialysis

A

Fatigue

Fluid restriction

Restricted diet – potassium, phosphate

Women are infertile

Reduced life expectancy

60
Q

Describe contraindications for transplant

A

Reduced life expectancy
> Older age
> Comorbidity

Surgical contraindications
> No bladder
> Calcified blood vessels

Medical contraindications
> Hypertension
> Hypotension
> Diseases that will recur in the transplant

61
Q

Describe the pathogenesis of transplant rejection

A

> Body recognises cell surface proteins as “non-self”
Blood group or HLA incompatibility

Pathogenesis of transplant rejection

> Foreign antigenic peptide recognised and bound by APC

> APC presents foreign antigenic peptide to T cell receptor and binds

> T cell activated, produces IL-2

> Leads to cascade of events and results in activation of T and B cells, as well as antibody production

Cell-mediated rejection
> Interstitial inflammation and tubulitis
> Treated with steroids
> Diagnosis – biopsy
> Does not present with proteinuria

Antibody-mediated rejection
> Endothelial swelling, glomerulitis and peritubular capillaritis
> Donor specific antibodies
> May present with proteinuria

62
Q

Describe the immunosuppressive agents used after transplantation

A

Basiliximab
> 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, inhibits proliferation

Steroids

63
Q

Describe the complications associated with immunosuppression

A

Rejection

Infection

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 jirovecii

Malignancy

> Kaposi sarcoma

> Skin: non-melanoma, non-epithelial; melanoma

> Non-Hodgkin & Hodgkin lymphoma

> Lung

> Kidney

> Colon and rectum

> Pancreas

64
Q

Define bacteriuria, giving risk factors and management plan

A

Bacteria in urine
Asymptomatic

Affects preschool age (girls > boys), adults (females > boys)

Other risk factors
> Urinary catheterisation
> Diabetes
> Anatomical abnormalities of urinary tract
> Pregnancy

Management

> Treat asymptomatic bacteriuria only in
> Preschool children
> Pregnancy
> Renal transplant
> Immunocompromised

> Treatment in other asymptomatic patients not indicated

65
Q

Describe the causes of UTI

A

> 95% caused by single organism

> Gram negative bacilli
> E. coli
> Klebsiella species
> Proteus species
> Pseudomonas species

> Gram positive bacteria
> Streptococcus species
» Enterococcus species
» S. Agalactiae (Group B streptococcus)

> > Staphylococcus species
> S. saprophyticus
> S. aureus

> Candida species
> Fungal balls
> Renal / peri-nephric abscesses

> Anaerobes
> Associated with bladder malignancies

Multiple organisms in
> Long-term catheteres
> Recurrent infections
> Structural / neurological abnormalities

Multi-drug resistant organisms
> Anatomical/neurological abnormalities
> Frequent infections
> Multiple antibiotic courses
> Prophylactic antibiotic use

66
Q

List the clinical features of a UTI

A

Suprapubic discomfort

Dysuria

Urgency

Frequency

Cloudy, blood-stained, smelly urine

Low-grade fever

Sepsis

Failure to thrive or jaundice in neonates

Abdominal pain and vomiting in children

Nocturia, incontinence and delirium in the elderly

67
Q

Describe the management of UTIs

A

Non-pregnant women
> First presentation, culture not mandatory
> Dipstick – high false positive rate
> Check previous culture results

Empirical antibiotic
> Amoxicillin, trimethoprim, nitrofurantoin
> Pivmecillinam, fosfomycin

No response to treatment
> Urine culture
> Change antibiotic

Children and men
> Send urine for every presentation
> Treat appropriately (empirical > targeted)

Pregnancy
> Send urine and treat each episode
> Check previous sensitivities > Amoxicillin and cefalexin relatively safe
> Avoid trimethoprim 1st trimester; avoid nitrofurantoin near term

Recurrent UTI
> Send sample from each episode
> Encourage hydration, urge-initiated and post-coital voiding
> Urology investigation
> Intravaginal/ oral oestrogen
> Antibiotic therapy as per symptoms

Catheter-associated UTI
> Colonisation common
> Biofilm production by bacteria
> Send CSU
> Start antibiotic – initially empirical based on previous microbiology
> Drug resistant and polymicrobial infections
> Remove / replace catheter

68
Q

Describe the symptoms of acute pyelonephritis as well as its management

A

Upper urinary tract infection
> Moderate to severe infection
> Flank pain +/- systemic infection
> Enlarged kidney
> Abscesses on surface of kidney (severe)

Management
> Urine
> Blood culture
> Imaging

Community
> Co-amoxiclav
> Ciprofloxacin
> Trimethoprim

Hospital

> IV antibiotics
> Amoxicillin / vancomycin
> Gentamicin / aztreonam / temocillin

> Uncomplicated pyelonephritis
7 day antibiotic course

Complicated pyelonephritis
> At least 2 weeks of antibiotics +/- radiological/surgical intervention (drainage of abscesses)

69
Q

Describe the complications of pyelonephritis

A

Renal abscess
> Complication of pyelonephritis – similar symptoms
> Positive urine and blood culture
> Usually gram negative bacilli

Can become life-threatening
> Emphysematous pyelonephritis
> Bubblewrap appearance
> Poor response to antibiotic therapy alone

Perinephric abscess
> Uncommon
> Often from haematogenous spread
> Common organisms
» Gram negative bacilli – E. coli, proteus species
» Gram positive cocci – S. aureus, streptococci
» Candida species

> Symptoms
> Similar to pyelonephritis
> Localised signs, local invasion

> Investigations
> Urine and blood cultures usually positive
> Pyuria +/- bacterial growth

> Poor response to antibiotic therapy – surgical management

70
Q

Describe acute bacterial prostatitis, including causes, signs and symptoms, complications, investigations and management

A

Usually spontaneous; may follow urethral instrumentation

Signs and symptoms
> Diffuse oedema
> Microabscesses
> Perineal / back pain
> UTI symptoms
> Urinary retention
> Pyrexia

Complications
> Prostatic abscess
> Spontaneous rupture – urethra, rectum
> Epididymitis
> Ascending infection
> Systemic sepsis

Investigations
> Urine and blood culture
> Transrectal US
> CT/MRI
> Do not obtain prostatic secretions

Likely organisms
> Gram negative bacilli – E. coli, proteus species
> S. aureus – MSSA, MRSA
> Neisseria gonnorhoea

Management
> Empirically ciprofloxacin / ofloxacin

71
Q

Describe chronic prostatitis

A

Rarely associated with acute prostatitis
> May follow Chlamydia urethritis

Signs and symptoms
> Recurrent UTI symptoms
> Perineal discomfort
> Back pain
> Low grade fever

Relapse common

Common organisms
> Gram negative bacilli – E. coli, proteus species
> Enterococcus species
> S. aureus – MSSA, MRSA

72
Q

Describe epidiymitis

A

Inflammatory reaction of the epididymis

Cause
> Ascending infection from urethra
> Urethral instrumentation

Symptoms
> Symptoms of UTI / urethritis
> Pain
> Fever
> Swelling
> Penile discharge

Common organisms
> GNB, enterococci, staphylococci
> TB in high risk areas and individuals
> Rule out Chlamydia and N. gonorrhoea in sexually active men

73
Q

Describe orchitis, including aetiology & signs and symptoms

A

Inflammation of one or both testicles

Signs and symptoms
> Testicular pain and swelling
> Dysuria
> Fever
> Penile discharge

Aetiology
> Usually viral – mumps

> Bacterial
> Pyogenic
> Complication of epididymitis
> IV antibiotics as per complicated UTI + surgical drainage

Complications
> Testicular infarction
> Abscess formation

74
Q

Describe Fournier’s gangrene including risk factors, investigations and management

A

Form of necrotising fasciitis
Usually >50 years of age
Rapid onset and spreading infection
Systemic sepsis

Risk factors
> UTI
> Complications of IBD
> Trauma
> Recent surgery

Common organisms
> Mixed infections – mainly GNB and anaerobes

Investigations
> Blood cultures
> Urine
> Tissue / pus

Management
> Surgical debridement
> Broad spectrum / combination antibiotics
> Piperacillin-tazobactam + gentamicin + metronidazole +/- clindamycin

75
Q

Describe the risk factors for prostate cancer

A

Age >65

Familial and genetic risk factors
> Especially first degree relatives
> Abnormalities on chromosomes 1q, 8p and Xp
> BRCA2 gene mutations
> PTEN and TP53 TSGs mutations

Hormones

Racial factors - increased risk in black population

Geographic variation - highest incidence in westernised nations

76
Q

What are the signs and symptoms of prostate cancer

A

Often asymptomatic

Painful or slow micturition

Urinary tract infection

Haematuria – blood in urine

Urinary retention – may cause anuria, uraemia

Lymphoedema

77
Q

Describe the metastatic complications of prostate cancer

A

Bone pain – most common symptom of metastases

Renal failure – ureteric obstruction
> Anorexia
> Weight loss
> Raised creatinine
> Stent or nephrostomy

Spinal cord compression
> Urological emergency – urgent MRI
> Severe pain
> Off legs
> Retention
> Constipation
> Radiotherapy v spinal decompression surgery

78
Q

Describe PSA and how it changes throughout life

A

PSA is a serine protease (33kD) secreted into seminal fluid

Responsible for liquefaction of seminal coagulation

Efficiently hydrolyses semenogelins causing release of sperm

Small proportion leaks into circulation

> Tends to rise with age
Depends on prostate size
Is influenced by inflammation and infection

79
Q

Describe the diagnosis and screening of prostate cancer

A

Digital rectal examination

PSA – prostate specific antigen

TRUS (trans-rectal ultrasound) – guided needle biopsy

80
Q

Describe the pathophysiology and grading of prostate cancer

A

Majority is primary adenocarcinoma

Usually arises in peripheral zone of prostate

Gleason grading

6 – well-differentiated, 25% likelihood of local progression

7– moderately differentiated, 50% likelihood of local progression

> 7 – poorly differentiated, 75% likelihood of local progression

81
Q

Describe the staging and treatment of prostate cancer

A

TNM classification
> T1 – within prostate
> T2 – felt on DRE
> T3 – cancer invades wall into seminal vesicles
> T4 – cancer invades adjacent organ i.e. bladder, bowel, pelvic floor

Localised prostate cancer
> Watchful waiting
> Active surveillance

> Radiotherapy (with or without LHRH analogue)
> External beam
> Conformal
> Brachytherapy

> Radical prostatectomy
Cryotherapy / HIFU
TURP if symptomatic

Advanced prostate cancer

> Androgen ablation therapy
> Medical castration – LHRH analogue
> Surgical castration – orchidectomy

Chemotherapy

TURP for relief of symptoms (transurethral resection of the prostate)

Radiotherapy

82
Q

List risk factors for bladder cancer

A

Age >50

Race – more common in Caucasians

Environmental carcinogens

Chronic inflammation
> Stones
> Infection – schistosomiasis
> Long-term catheters

Drugs – phenacitin, cyclophosphamide

Pelvic radiotherapy

Occupation

Smoking – especially from 4-ABP and naphythylamines

83
Q

Describe the presentation and investigations used in bladder cancer

A

Presentation / diagnosis
> Classically painless frank haematuria

Investigations
> Cystoscopy
> Renal US
> CT KUB

84
Q

List the different types of bladder cancer

A

Transitional cell carcinoma (90%)
> Superficial – 75%
> Invasive – 25%

Squamous carcinoma (5%)

Adenocarcinoma (2%)

Other secondaries

Muscle invasive bladder cancer is highly aggressive

85
Q

Describe the treatment of bladder cancer

A

> Diagnosed at flexible cystoscopy
Urgent TURBT (trans-urethral resection of bladder tumour)
CT IVU
Bimanual examination carried out at TURBT
Intravesical mitomycin reduces risk of recurrence

Low-grade superficial TCC
> Flexible check cystoscopy 3 months
> 30% chance of recurrence
> Course of 6 weekly mitomycin treatment given for persistent Ta tumours

High-grade non-muscle-invasive bladder cancer (HG NMIBC)
> 80% recurrence risk; 50% chance of progressing to muscle invasive disease
> Do early check cystoscopy and rebiopsy
> Treat with intravesical BCG immunotherapy – effective in 50%
> Course of 6 weekly instillations then further cystoscopy/biopsy
> Cystectomy if treatment fails

MIBC
> Requires radical therapy
> Radical cystectomy or radiotherapy
> Bladder and prostate/uterus removed
> Urine diverted into an ileal conduit or rarely an orthotopic neobladder
> Neo-adjuvant chemotherapy

Metastatic disease
> Often pulmonary
> Treat with chemotherapy
> Classic M-VAC
» Methotrexate
» Vinblastine
» Doxorubicin
» Cisplatin
> Gemicitobine / docetaxel

86
Q

Describe the types of renal cell carcinoma and associated risk factors

A

85% of all renal tumours

Others
> Transitional cell carcinoma
> Sarcoma
> Metastases

Risk factors
> Smoking
> Obesity
> Hypertension
> Acquired renal cystic disease
> Haemodialysis

Genetics
> VHL (Von Hippel Lindau)
> HPRCC – hereditary papillary renal carcinoma
> HLRCC – hereditary leiomyomatosis and renal cell cancer
> Birt-Hogg-Dube
> Tuberous sclerosis

87
Q

Describe the presentation of renal cell carcinoma

A

Incidental

Systemic symptoms
> Night sweats
> Fever
> Fatigue
> Weight loss
> Haemoptysis

Classic triad
> Mass
> Pain
> Haematuria

> Varicocoele

> Lower limb oedema

> Paraneoplastic syndrome
> Polycythaemia due to increased EPO
> Hypercalcaemia due to PTHrP or from osteolytic hypercalcaemia
> Hypertension due to renin secretion
> Deranged LFTs – Stauffer’s syndrome – due to hepatotoxic tumour products

88
Q

Describe the histology and staging of renal cell carcinoma

A

Histology
> Clear cell (80%)
» Vascular, granular and clear (lipids)

> Papillary
Chromophobe – large polygonal
Collecting duct – rare
Medullary cell – rare

Staging - TNM staging
> T3a – invasion into renal vein
> T3B – IVC below diaphragm
> T3c – IVC above diaphragm
> T4 – beyond Gerota’s and adrenal gland

89
Q

Describe the treatment of renal cell carcinoma

A

Radical nephrectomy (includes Gerota’s fascia, spares adrenal gland)
> Large renal mass
> If no absolute indication for nephron-sparing surgery (NSS)

Indications for NSS
> Single kidney
> CKD
> CV risk factors
> pT1a tumours

Small renal mass
> Biopsy

> Treatment

> > NSS
> Partial nephrectomy
> Cryotherapy

> > Radical nephrectomy

> > Surveillance

> Metastatic disease - tyrosine kinase inhibitors

90
Q

Describe the risk factors and presentation of testicular cancer

A

Most common solid cancer in younger men (20-45)
Most curable cancer

Risk factors
> Age 20-45
> Cryptorchidism
> HIV
> Caucasian population

Clinical presentation
> Painless lump

91
Q

Describe the investigations and classification of testicular cancer

A

Scrotal ultrasound

Tumour markers
> Alpha-fetoprotein – teratomas and yolk sac tumours
> Beta hCG – teratoma, seminoma
> LDH – seminoma

Classification
> Germ cell tumours
> Seminoma
> Teratoma
> Mixed
> Yolk sac

Stromal tumours
> Leydig
> Sertoli

Other
> Lymphoma
> Metastasis

92
Q

Describe the treatment of testicular cancer

A

Radical orchidectomy

Chemotherapy

Para-aortic nodal radiotherapy

Retroperitoneal lymph node dissection

93
Q

Describe penile cancer and its treatment

A

Rare
Associated with HPV infection (16, 18, 21) and smoking
Premalignant lesions – chronic changes
Even rarer in males circumcised at birth

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

94
Q

Describe the position, size and surrounding fascia of the kidneys

A

Paired retroperitoneal organs (T12-L3))
Right lies lower than left; normally 10-12cm in length, 5-7cm wide and 3cm thick
Surrounded by Gerota’s fascia

Clinically important

> For PCNL (percutaneous nephrolithotomy)
> Upper pole more posterior and medial
> Medial surface more anterior

> Gerota’s fascia deficient inferiorly
> Often where haemorrhage or haematoma can appear after trauma

95
Q

Describe the anatomy of the ureters including layers and physiological narrowings

A

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
> Urothelial mucosa
> Lamina propria
> Muscular layer
> Adventitial layer

3 physiological narrowings

> Pelviureteric junction (PUJ)

> Ureters cross iliac vessels at pelvic brim (midureter)

> Vesicoureteric junction (VUJ)
> Ureter joins bladder

96
Q

Describe the risk factors for urolithiasis

A

Intrinsic

> Sex (male:female 2:1)
> Testosterone increases production of oxalate
> Females produce more citrate (productive)

> Age: peak 20-50 years

> Family history
> More common in Caucasian, Asian
> Familial renal tubular acidosis
> Cystinuria

> Comorbid factors

Extrinsic

> Fluid intake

> Diet
> High animal protein
» High oxalate, low pH, low citrate
> High salt – hypercalciuria
>Low calcium diets

> Sedentary lifestyle

> High incidence in hot climates

> Country of residence

97
Q

Describe the different types of kidney stones

A

Calcium oxalate stones most common
> Radio-opaque: seen on X-ray

Uric acid
> Form due to chronic dehydration
> Increased risk with gout, genetic tendency, diet with excess protein

Calcium phosphate + calcium oxalate

Pure calcium phosphate
> Rare
> May be seen in renal tubular acidosis

Struvite
> Seen in UTIs
> Consist of magnesium, ammonium and phosphate
> Require aggressive treatment of UTI

Cysteine
> Rare, predominantly associated with cysteinuria (genetically inherited condition)

Xanthine
> Enzyme deficiency causes buildup of xanthine deposits

Silica
> Rare
> Caused by medications or herbal supplements

98
Q

Describe the pathogenesis of urolithiasis

A

Undersaturated

Supersaturated but stable – metastable

Supersaturated with spontaneous precipitation – unstable

Saturation product
> level at which no more solute will dissolve in a solution without a change in pH, temperature

Formation product – level at which spontaneous formation occurs

Free particle model of stone formation
> Crystals growing and agglomerating
> Critical particle trapped in tubule

Fixed particle model of stone formation
> Crystals growing and agglomerating
> Particle adheres to a damaged site on the tubule wall and other crystals agglomerate with it

99
Q

Describe the presentation of kidney stones

A

Incidental

Pain
> Colic
> Radiates from loin to groin
> In males can be testicular or penile pain
> Cannot settle
> Unable to stay still

Haematuria
> Visible or non-visible

Sepsis/infection
> Unknown source until imaged

DDX
> AAA
> Appendicitis
> Gynae pathology

100
Q

Describe the investigations used for kidney stones

A

History and examination

Bloods
> U&Es, CRP, FBC

Urine
> Dipstick

MSSU
> Calcium
> Urate
> Sodium nitroprusside – cystine

Stone analysis

Imaging
> Gold standard – CT KUB
» Stone diameter
» Skin to stone distance

> Ultrasound
> Especially young females

> X-ray
> Better for follow-up of known radioopaque stone

101
Q

Describe the treatment of

A

Analgesia
> NSAIDs – reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis

Tamsulosin
> Alpha blocker which blocks muscle contraction
> Relaxes ureter and encourages stone passage

Surgical options

> Ureteroscopy and basket

> Ureteroscopy and fragmentation

> FURS – flexible ureteroscopy

> ESWL – extracorporeal shockwave lithotripsy

> PCNL – percutaneous nephrolithotomy

Evidence of sepsis

> Retrograde ureteric stent
> Inserted by urology under anaesthetic
> Connects bladder to kidney

> Nephrostomy
> Inserted percutaneously by interventional radiology in an antegrade fashion

102
Q

Describe ESWL

A

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 enter stone causing fragmentation

103
Q

Describe staghorn calculi and how they are formed

A

Branched stones that fill all or a part of the renal pelvis and branch into several or all of the calyces

Most often composed of struvite
> Bacteria produce urease, breaks down urea into ammonia
> Causes alkalinisation of urine and formation of magnesium ammonium phosphate crystals

104
Q

Describe percutaneous nephrolithotomy (PCNL)

A

Creates a percutaneous tract from skin to kidney

Able to clear larger volumes of stone e.g. struvite

Increased risk as it is an invasive procedure

105
Q

Describe the fluid compartments of the body

A

Intracellular
> 2/3 of fluid

> Composition: potassium

Extracellular
> 1/3 of fluid
> Composition

> > Interstitium: sodium, chloride

> > Plasma (intravascular)

106
Q

Describe third space losses and risks associated with osmolar problems

A

Third space losses
> More fluid in extracellular compartment than there should be
e.g. low albumin in intravascular space – fluid taken into interstitium
> Interstitial space becomes overexpanded

Risk of osmolar problems

> Cerebral oedema
> Acute hyponatraemia

> Osmotic demyelination syndrome
> Sodium corrected too quickly

107
Q

Describe signs and symptoms associated with fluid depletion and fluid overload

A

Relevant history
> Fluid depletion – diuretics, abnormal losses
> Fluid overload - heart failure, renal failure

Symptoms
> Fluid depletion – postural hypotension, thirst, dry mouth
> Fluid overload – breathlessness, swollen ankles

Signs
> Fluid depletion – reduced skin turgor, CRT >2 secs, tachycardia
> Fluid overload – hypertension, increased JVP, 3rd heart sound, pulmonary oedema

Lab tests
> Fluid depletion - U&Es, especially high urea
> Fluid overload – serum albumin

108
Q

Describe the NICE guidelines’s 5 R’s

A

Resuscitation
> Restore circulation to vital organs following loss of intravascular volume

Clinical signs of hypovolaemia
> Hypotension
> Tachycardia
> Peripherally cool
> CRT > 2 secs
> NEWS > 5

Passive leg raising suggests fluid responsiveness

Fluid bolus, usually saline or Hartmann’s

Routine maintenance
> Patients not drinking / unable to drink / having to fast for over 8-12h

> Calculate requirement based on
> Projected losses
> Intake e.g. IV drug volumes / NG feed

Replacement
> Treat deficits or ongoing losses not needed urgently for resus

Redistribution

Reassessment
> Daily U&Es and fluid balance
> Consider daily bicarbonate or magnesium if abnormal GI or renal losses

109
Q

Describe the different types of IV fluids

A

Crystalloids

> Saline (various, 0.9% is standard)
> Distributes between extracellular compartments

> Dextrose (various, 5% is standard)
> goes straight into intracellular compartments

> Balanced solutions e.g. Hartmann’s or Ringer’s lactate
> Distributes between extracellular compartments

> Sodium bicarbonate (1.26%) - expert advice only

Colloids
> E.g. Gelofusion or starch-based fluid
> Stay in intravascular space

Blood products
> Packed red cells
> Platelets or fresh frozen plasma (clotting factors)
> Human albumin solution

110
Q

Describe the KDIGO criteria for AKI

A

Severity of AKI – KDIGO

Stage 1
> Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline

Stage 2
> Serum creatinine >2.0 and <3x AKI baseline

Stage 3
> Serum creatinine 3x AKI baseline or >354 micromol/l increase above AKI baseline

111
Q

State why peritoneal dialysis can cause hyperglycaemia

A

The dialysate contains dextrose.
Absorbing some of the dialysate might cause the consumption of hundreds of extra calories daily, leading to hyperglycaemia and weight gain.

112
Q

Discuss why nephrotic syndrome can increase risk of DVT

A

Antithrombin II deficiency can be inherited or acquired.
The patient has nephrotic syndrome, which is associated with a loss of antithrombin III from the kidneys resulting in an acquired deficiency and a hypercoagulable state and thus puts this patient at risk of the development of deep vein thrombosis.

113
Q

Discuss presentation and management of renal carcinoma

A

Painless flank mass, haematuria, and paraneoplastic features including hypertension, polycythaemia, hypercalcaemia, and Cushing’s syndrome

Localised renal cancer (that is 7 cm or larger) is definitively treated with a radical nephrectomy. Adjuvant treatment does not help completely resected disease

114
Q

List characteristics of Wegener granulomatosis

A

elevated serum creatinine level
sinusitis
hematuria
pleural effusions
positive result of antineutrophil cytoplasmic antibody test

115
Q

What bacteria infection is commonly associated with peritoneal dialysis

A

staphylococcus epidermis

116
Q

State the difference in onset after respiratory infection in PSGN and IgA nephropathy

A

IgA nephropathy would occur a few days after the respiratory infection rather than weeks.

117
Q

State the first line analgesia in renal colic

A

IM diclofena

Phase 3 (14 decks)

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