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Karteikarten

Nephrology: AKI

Ellie Britt Year 4 Medicine Englisch 59 Karten

RIFLE classification of AKI

Karten in diesem Stapel (59)

  1. 1definition of acute kidney injurySignificant decline in renal function over hrs or days manifesting as an abrupt and sustained ↑ in Se U and Cr
  2. 2causes of AKIPre-renal and ATN account for ~80%
    Pre-renal: commonest cause
     Shock or renovascular compromise (e.g. NSAIDs, ACEi)
    Renal
     ATN:
     Ischaemia: shock, HTN, HUS, TTP
     nephrotoxins: drugs, contrast, Hb
     Acute TIN: drug hypersensitivity
     Nephritic syndrome
    Post-renal: SNIPPIN
  3. 3presentation of AKI Uraemia
     Acidosis
     Hyperkalaemia
     Fluid overload
  4. 4clinical assessment in AKI1. Acute or chronic?
     Can’t tell for sure: Rx as acute
     Chronic features
    - Hx of comorbidity: DM, HTN
    - Long duration of symptoms
    - Previously abnormal bloods (GP records)
    2. Volume depleted?
     Postural hypotension
     ↓ JVP, ↑ pulse
     Poor skin turgor, dry mucus membranes
    3. GU tract obstruction?
     Suprapubic discomfort
     Palpable bladder
     Enlarged prostate
     Catheter
     Complete anuria (rare in ARF)
    4. Rare cause?
     Assoc. c¯ proteinuria ± haematuria
     Vasculitis: rash, arthralgia, nosebleed
  5. 5Ix in AKI Bloods: FBC, U+E, LFT, glucose, clotting, Ca, ESR
     ABG: hypoxia (oedema), acidosis, ↑K+
     GN screen: if cause unclear
     Urine: dip, MCS, chemistry (U+E, PCR, osmolality, BJP)
     ECG: hyperkalaemia
     CXR: pulmonary oedema
     Renal US: Renal size, hydronephrosis
  6. 6urine in pre-renal failurein pre-renal failure, urine is concentrated and Na is reabsorbed → ↑osmolality, Na <20mM
  7. 7RIFLE classification of AKIRIFLE classification of AKI
  8. 8General Mx in AKI - stop what? Identify and Rx pre-renal or post-renal causes
     Urgent US
     Rx exacerbating factors: e.g. sepsis
     Give PPIs
     Stop nephrotoxins: NSAIDs, ACEi, gent, vanc
     Stop metformin if Cr > 150mM
  9. 9urea-creatinine ratio and causes0-100:1 – normal or post renal cause of AKI
    >100:1 – pre-renal cause (urea absorption increased compared to creatinine)
    <40:1 – intrinsic renal damage (urea unable to be absorbed -> become like creatinine -> ratio gets closer to 1)
  10. 10Monitoring in AKI Catheterise and monitor UO
     Consider CVP
     Fluid balance
     Wt.
  11. 11Management of hyperkalaemia 10ml 10% calcium gluconate
     50ml 50% glucose + 10u insulin (Actrapid)
     Salbutamol 5mg nebulizer
     Calcium resonium 15g PO or 30g PR (slow)
     Haemofiltration (usually needed if anuric)
  12. 12Pulmonary oedema Mx Sit up and give high-flow O2
     Morphine 2.5mg IV (± metoclopramide 10mg IV)
     Frusemide 120-250mg IV over 1h
     GTN spray ± ISMN IVI (unless SBP <100)
    If no response consider:
     CPAP
     Haemofiltration / haemodialysis ± venesection
  13. 13Bleeding in AKI - why - Mx ↑ urea impairs haemostasis
     FFP + plats as needed
     Transfuse to maintain Hb >10
  14. 14indications for acute dialysis1. Persistent hyperkalaemia (>7mM)
    2. Refractory pulmonary oedema
    3. Symptomatic uraemia: encephalopathy, pericarditis
    4. Severe metabolic acidosis (pH <7.2)
    5. Poisoning (e.g. aspirin)
  15. 15assessing fluid statusCV: postural BP, JVP, HR
    tissues: CRT, cold/warm hands, skin turgor, mucus membranes
    end-organ: mental state, urine output
  16. 16Rx of shock/dehydration in AKI Fluid challenge 250-500ml over 30min
     Repeat as necessary: aim for CVP of 5-10cm
     Once replete, continue @ 20ml+UO/h
  17. 17Acute Renal Failure Mx flowchart1. resuscitate and assess fluid status
    2. Rx life-threatening complications
    3. Rx shock or dehydration
    4. Monitor
    5. look for evidence of post-renal causes
    6. Hx and Ix
    7. blood cultures and empirical Abx if septic
    8. further Mx: nephrology
  18. 18What is acute interstitial/tubulointerstitial nephritis?Immune-mediated hypersensitivity c¯ either drugs or other Ag acting as haptans
  19. 19causes of interstitial nephritisDrug hypersensitivity in 70%
     NSAIDs
     Abx: Cephs, penicillins, rifampicin, sulphonamide
     Diuretics: frusemide, thiazides
     Allopurinol
     Cimetidine
    Infections in 15%
     Staphs, streps
    Immune disorders
     SLE, Sjogren’s
  20. 20presentation of interstitial nephritis Fever, arthralgia, rashes
     AKI → olig/anuria
     Uveitis
  21. 21Ix and Rx in interstitial nephritisIx
     ↑IgE, eosinophilia
     Dip: haematuria, proteinuria, sterile pyuria
    Rx
     Stop offending drug
     Prednisolone
    Prognosis: Most recover renal function
  22. 22Chronic TINFibrosis and tubular loss
    Commonly caused by:
     Reflux and chronic pyelonephritis
     DM
     SCD or trait
  23. 23Acute Urate Crystal Nephropathy - why - Rx AKI due to urate precipitation
     Usually after chemo-induced cell lysis, gout
     Rx: hydration, urinary alkalinisation
  24. 24Nephrocalcinosis - what - causes Diffuse renal parenchymal calcification
     Progressive renal impairment
    Causes
     Malignancy
     ↑PTH
     Myeloma
     Sarcoidosis
     Vit D intoxification
    Renal Tubular Acidosis
  25. 25How do nephrotoxins cause kidney damage? Either directly toxic → ATN
     Or cause hypersensitivity → TIN
  26. 26exogenous nephrotoxins NSAIDs
     ACEi
     Immunosuppressants: (Ciclosporin, Tacrolimus)
     Contrast media
     Anaesthetics: enflurane
    Antimicrobials: AVASTA
     Aminoglycosides
     Vancomycin
     Aciclovir
     Sulphonamides
     Tetracycline
     Amphotericin
  27. 27Endogenous nephrotoxins Haemoglobin, myoglobin
     Urate
     Ig: e.g. light chains in myeloma
  28. 28pathogenesis of rhabdomyolysisSkeletal muscle breakdown → release of:
     K+, PO4, urate
     Myoglobin, CK
    ↑K and AKI
  29. 29causes of rhabdomyolysis Ischaemia: embolism, surgery
     Trauma: immobilisation, crush, burns, seizures, compartment syndrome
     Toxins: statins, fibrates, ecstasy, neuroleptics
  30. 30clinical and investigation findings in rhabdomyolysisClinical
     Muscle pain, swelling
     Red/brown urine
     AKI occurs 10-12h later
    Ix
     Dipstick: +ve Hb, -ve RBCs
     Blood: ↑CK, ↑K, ↑PO4, ↑urate
  31. 31Rx of rhabdomyolysis Rx hyperkalaemia
     IV rehydration: 300ml/h
     CVP monitoring if oliguric
     IV NaHCO3 may be used to alkalinize urine and stabilise a less toxic form of myoglobin.
  32. 32features of chronic renal failure Kidney damage ≥3mo indicated by ↓ function
     Symptoms usually only occur by stage 4 (GFR<30)
     ESRF is stage 5 or need for RRT
  33. 33classification of CKD1: eGFR >90
    2. 60-89
    3a. 45-59
    3b: 30-44
    4. 16-29
    5: <15
  34. 34causes of CKDCommon
     DM
     HTN
    Other
     RAS
     GN
     Polycystic disease
     Drugs: e.g. analgesic nephropathy
     Pyelonephritis: usually 2O to VUR
     SLE
     Myeloma and amyloidosis
  35. 35important points in Hx-taking in CKD Past UTI
     HTN, DM
     FH
     DH
     Symptoms
  36. 36non-radiological Ix in CKDBlood
     ↓Hb, U+E, ESR, glucose, ↓Ca/↑PO4, ↑ALP, ↑PTH
     Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep
     Film: burr cells
    Urine: dip, MCS, PCR, BJP
    Renal biopsy: if cause unclear and size normal
  37. 37imaging in CKD CXR: cardiomegaly, pleural/pericardial effusion, oedema
     AXR: calcification from stones
     Renal US
    - Usually small (<9cm)
    - May be large: polycystic, amyloid
     Bone X-rays: renal osteodystrophy (pseudofractures)
     CT KUB: e.g. cortical scarring from pyelonephritis
  38. 38complications of CKDCRF HEALS
     Cardiovascular disease
     Renal osteodystrophy
     Fluid (oedema)
     HTN
     Electrolyte disturbances: K, H
     Anaemia
     Leg restlessness
     Sensory neuropathy
  39. 39Renal Osteodystrophy mechanism ↓ 1α-hydroxylase → ↓ vit D activation → ↓ Ca → ↑ PTH
     Phosphate retention → ↓ Ca and ↑ PTH (directly, secondary hyperparathyroidism)
     ↑ PTH → activation of osteoclasts ± osteoblasts
     Also acidosis → bone resorption
  40. 40features of renal osteodystrophy Osteoporosis: ↓ bone density
     Osteomalacia: ↓ mineralisation of osteoid (matrix)
    2O/3O HPT → osteitis fibrosa cystica
    - Subperiosteal bone resorption
    - Acral osteolysis: short stubby fingers
    - Pepperpot skull
     May get spinal osteosclerosis
  41. 41general and lifestyle measures in CKDGeneral
     Rx reversible causes
     Stop nephrotoxic drugs
    Lifestyle
     Exercise
     Healthy wt.
     Stop smoking
     Na, fluid and PO4 restriction
  42. 42Mx in CKD of: - CV risk - HTN - oedemaCV Risk
     Statins (irrespective of lipids)
     Low-dose aspirin
     Rx DM
    Hypertension
     Target <140/90 (<130/80 if DM)
     In DM kidney disease give ACEi/ARB (inc. if normal BP)
    Oedema
     Frusemide
  43. 43Mx of bone disease in CKD Phosphate binders: sevelamer, calcichew
     Vit D analogues: alfacalcidol (1 OH-Vit D3)
     Ca supplements
     Cinacalcet: Ca mimetic
  44. 44Mx of anaemia in CKD Exclude IDA and ACD
     EPO to raise Hb to 11g/dL (higher = thrombosis risk)
  45. 45Mx of restless legs in CKD Clonazepam
  46. 46contraindications to renal transplant Active infection
     Cancer
     Severe HD or other co-morbidity
  47. 47types of graft in renal transplant Cadaveric: brainstem death c¯ CV support
     Non-heart beating donor: no active circulation
    Live-related
    - Optimal surgical timing
    - HLA-matched
    - Improved graft survival
     Live unrelated
  48. 48immunosuppresion in renal transplant????????
  49. 49acute complications in renal transplantPost-op
     Bleeding
     Graft thrombosis
     Infection
     Urinary leaks
    Hyperacute rejection (minutes)
     ABO incompatibility
     Thrombosis and SIRS
    Acute Rejection (<6mo)
     ↑ing Cr (± fever and graft pain)
     Cell-mediated response
     Responsive to immunosuppression
  50. 50chronic complications of renal transplantChronic Rejection (>6mo)
     Interstitial fibrosis + tubular atrophy
     Gradual ↑ in Cr and proteinuria
     Not responsive to immunosuppression
    Ciclosporin / tacrolimus nephrotoxicity
    - Acute: reversible afferent arteriole constriction → ↓GFR
    - Chronic: tubular atrophy and fibrosis
    ↓ Immune Function
     ↑ infection: opportunists, fungi, warts
     ↑ risk of malignancy: BCC, SCC, lymphoma (EBV)
    Cardiovascular Disease
     Hypertension and atherosclerosis
  51. 51Diabetic nephropathy pathology Diabetic nephropathy describes conglomerate of lesions
    occurring concurrently:
     Hyperglycaemia → renal hyperperfusion → hypertrophy
    and ↑ renal size
     Hypertrophy and metabolic defects inc. ROS production → glomerulosclerosis and nephron loss
     Nephron loss → RAS activation → HTN
  52. 52Diabetic nephropathy clinically Microalbuminuria (30-300mg/d or albumin:creatinine >3)
    ( Strong independent RF for CV disease)
     Progresses to proteinuria (albuminuria >300mg/d)
     Diabetic retinopathy usually co-exists and HTN is common
  53. 53diabetic nephropathy screeningT2DMs should be screened for microalbuminuria 6moly
  54. 54Rx fo diabetic nephropathy Good glycaemic control delays onset and progression
     BP target 130/80
     Start ACEi/ARB even if normotensive
     Stop smoking
     Combined kidney pancreas Tx possible in selected pts
  55. 55Amyloidosis - features - DxRenal involvement usually caused by AL/AA amyloid
    Features:
     Proteinuria
     Nephrotic syndrome
     Progressive renal failure
    Dx
     Large kidneys on US
     Biopsy
  56. 56Maliganancy and renal diseaseDirect
     Renal infiltration: leukaemia, lymphoma
     Obstruction: pelvic tumour
    Mets
     Nephrotoxicity
     Toxic chemo
     Analgesics
     Tumour lysis syndrome
  57. 57How does sarcoidosis cause renal disease?↑ Ca and TIN
  58. 58Myeloma and renal disease - pathology - presentation - RxPathology
     Excess production of monoclonal Ab ± light chains (urinary BJP in 60%).
     Light chains block tubules and have direct toxic effects → ATN.
     Myeloma also assoc. c¯ ↑↑Ca2+
    Presentation
     ARF / CRF
     Amyloidosis
    Rx
     Ensure fluid intake of 3L/d to prevent further impairment
     Dialysis may be required in ARF
  59. 59Berger's diseasegross haematuria, a history of symptoms suggestive of an upper respiratory tract infection and a purpuric skin lesion resembling Henoch Schonlein Purpura.
    This collection of symptoms is suggestive of Berger's disease (also known as IgA Nephropathy)

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Year 4 Medicine Karteikarten am Nephrology: AKI, erstellt von Ellie Britt am 12/12/2018.
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Ellie Britt
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