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Flashcards

CKD

Anna Hogarth Met3B English 32 cards

Cards in this deck (32)

  1. 1Define CKDAbnormal kidney structure or function, present for >3 months with implications for health.
    Can be classified by eGFR, presence of albuminuria, and the cause of kidney disease
  2. 2What are the gradings of CKD based on GFR?G1: >90 - Only CKD if other evidence of kidney damage
    G2: 60-89 - Only CKD if other evidence of kidney damage
    G3a: 45-59 - Mild to moderate
    G3b: 30-44 - Moderate to severe
    G4: 15-29 - Severe
    G5 < 15 - Kidney failure
  3. 3What are the classifications of CKD based on albumin excretion (mg/24hr) and albumin:creatinine ratio (mg/mmol)?A1: <30mg/24hr and A:Cr <3mg/mmol
    A2: 30-300mg/34hr
    A3: >300 and A:Cr>30mg/mmol
  4. 4What are the most common causes of CKD?Diabetes (24%)
    Glomerulonephritis (13%)
    Raised BP/renovascular disease (11%)
  5. 5How does diabetes contribute to CKD?Hyperglycaemia leads to increased growth factors, RAAS activation, production of glycosylation end-products, and oxidative stress. This in turn leads to an increase in glomerular capillary pressure, podocyte damage and endothelial dysfunction.
  6. 6What is the first sign of kidney damage in diabetes?Albuminuria
  7. 7What are the key pathologies that lead to a loss of kidney function in diabetes?Glomerulosclerosis, nodule formation (Kimmelstiel-Wilson lesion), and fibrosis with progressive loss of renal function. Co-existing high blood pressure increases the progression of the disease
  8. 8How is diabetic nephropathy diagnosed? How often are diabetic patients screened?Microalbuminuria = A:Cr of 3-30mg/mmol - THIS IS NOT DETECTABLE WITH A STANDARD DIPSTICK, MUST SEND FOR A:Cr screen. Screen annually
  9. 9What are the systemic effects of CKD?1) Metabolic acidosis
    2) Volume overload
    3) Hyperkalaemia
    4) Hypertension
    5) Anaemia
    6) Hyperparathyroidism, hypocalcaemia, hypophosphataemia
  10. 10When should a referral to nephrology be made?1) Stage G4 or G5 CKD
    2) Moderate proteinuria A:CR > 70mg/mmol unless for DM and already treated
    3) Proteinuria A:Cr > 30mg/mmol with haematuria
    4) Declining eGFR: decrease in eGFR>25% + a drop in GFR category or a sustained eGFR decrease of 15% over 12 months
    5) High BP poorly controlled despite >4 antihypertensive drugs at therapeutic dose
    6) Known or suspected rare or genetic cause of CKD
  11. 11What four systems are targeted to slow renal disease progression?BP
    RAAS
    Glycaemic control
    Lifestyle
  12. 12What are the BP targets for slowing down the progression of renal disease?<140/90
    <130/80 if DM or A:Cr >70mg/mmol
  13. 13When are ARB or ACE-i offered to slow progression of renal disease?1) DM and A:Cr >3mg/mmol
    2) Hypertension and A:Cr >30mg/mmol
    3) Any CKD with A:Cr >70mg/mmol
  14. 14Why can two RAAS antagonists not be combined?Risk of hypotension and hyperkalemia
  15. 15What needs to be checked before commencing and ACE-i or ARB? And monitored? What are the criteria for stopping a RAAS antagonist?1) Check K+ and renal function before commencing
    2) Check K+ and renal function 1-2 weeks after starting treatment or changing dose
    3) Stop if K+ >6mmol/L, decrease in eGFR by 25% or a decrease in creatinine of more than 30%
  16. 16What is the target HbA1c in CKD? What are the exceptions?53mmol/mol
    Unless risk of hypoglycaemia, comorbidity or limited life expectancy
  17. 17What general lifestyle advice should be given to slow progression of CKD?Exercise, healthy weight, and smoking cessation. Dietary salt intake should be <2g sodium per day
  18. 18How is anaemia managed?Check Hb when eGFR is <60 - investigate and check other deficiencies i.e. iron deficiency (hypochromic, microcytic), B12 and folate (macrocytic). Consider treatment with EPO stimulating agent (ESA) if Hb <110g/L and likely to benefit in terms of function and quality of life
  19. 19What is a very severe and rare complication of ESA?Red cell aplasia due to anti-EPO antibodies and usually causes an Hb <60g/L
  20. 20How is acidosis managed in CKD?Consider sodium bicarbonate supplements for patients with eGFR of <30 and low serum bicarbonate (<20mmol/L). Caution in patients with hypertension and fluid overload due to sodium component.
  21. 21How is oedema managed in CKD?Restrict fluid and sodium intake - can use a loop and thiazide diuretic. Diuretic treatment should only be given with careful monitoring of fluid state and renal function.
  22. 22What impact does CKD have on bone mineral-disorders?Increases serum phosphate and reduces hydroxylation of Vitamin D
  23. 23How does CKD cause secondary hyperparathyroidism? How does this lead to tertiary?Reduction of active vitamin D formation leads to a reduction in serum calcium (due to reduced GI absorption). As a consequence there is an increase parathyroid hormone release. In the chronic setting, the baseline for PTH release is lowered and the parathyroid gland enlarges. Once serum calcium levels are restored, the gland is now so enlarged that continues to produce massive amounts of PTH
  24. 24What are the effects of PTH release?1) Increase in 1a-hydroxylase activity - increased absorption of calcium from gut, reduced phosphate excretion, increased osteoblast activity
    2) Increased osteoclast activity
    In CKD, renal function is impaired so vitamin D can't be produced - this results in hyperphosphatemia (no renal excretion) and an increased efflux of calcium from bone
  25. 25When are bone-mineral disorders investigated in CKD?Measure calcium, phosphate, ALP, PTH and 25-OH vit D if eGFR is <30
  26. 26When/how is hyperphosphatemia managed?Treat if phosphate >1.5mmol/L (>1.7mmol/L if RRT) with dietary restrictions +/- phosphate binders. Use of binders which do not contain calcium may be beneficial in preventing vascular calcification
  27. 27How is low vitamin D managed?Give vit D supplements (colecalciferol, ergocalciferol). If high PTH persists then treat with activated vitamin D analogue e.g. 1a-calcidol or calcitriol.
    Paricalcitol suppresses PTH with less effect on gut absorption of calcium and phosphate and is less likely to cause high calcium/phosphate
  28. 28How is restless leg/cramps managed?Exclude iron-deficiency as a possible factor. Give sleep hygiene advice.
    Treatment with gabapentin/pregabalin/dopamine agonists if off licence and may be complicated with side effects (falls, cognitive impairments, impulse-control disorder)
  29. 29What dietary advice is given to manage complications?Expert advice regarding protein intake, K+ if hypertensive, and phosphate reduction (i.e. dairy products)
  30. 30Why does CKD increase the risk of CVD?Raised blood pressure
    Vascular stiffness
    Inflammation
    Oxidative stress
    Abnormal endothelial function
  31. 31How is CVD risk managed in CKD?1) Antiplatelets - for CKD at risk for atherosclerotic events (weigh up bleeding risk)
    2) Atorvastatin 20mg for primary and secondary prevention of CVD
    3) CKD should not affect treatment for heart failure but increase monitoring of GFR and K+
    4) GFR < 60 mat affect troponin and BNP values. Interpret results cautiously.
  32. 32Which classes of drugs do you need to alter the dose of in CKD? (7)1) Aminoglycosides
    2) Heparin
    3) Opiates
    4) Digoxin
    5) Cephalosporins
    6) Lithium
    7) Penicillins
    In chemotherapy, an exact measurement of GFR must be taken

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Met3B (Renal Medicine) Flashcards on CKD, created by Anna Hogarth on 13/02/2020.
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Anna Hogarth
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