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RENAL > C. AKI > Flashcards

C. AKI Flashcards

1
Q

what does the urinary system consist of

A
  • 2 kidneys
  • 2 ureters
  • a single midline urinary bladder
  • single urethra
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2
Q

what are the functions of the kidney

A
  • regulating blood volume & blood pressure (RAAs system)
  • regulating plasma concentration of ions (acids and bases)
  • maintaining plasma pH
  • conserving valuable nutrients like N-based: urea, NO (ie. through kidney)
  • elimination of toxic/unwanted substances
  • adjusting red blood cell count in response to oxygen
    demand (EPO from bone marrow)
  • maintenance of calcium and phosphate balance (kidney activates vitamin D)
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3
Q

why is AKI important

A
  • can progress to CKD which is irreversible
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4
Q

signs and symptoms of AKI

A
  • may be asymptomatic (look at blood results)
  • reduced urine output or anuria
  • change in urine appearance
  • change in urine smell
  • swelling in ankles, legs or around the eyes
  • fatigue or tiredness
  • shortness of breath
  • nausea and vomiting
  • abdominal pain
  • dehydration and thirst
  • seizure or coma
  • chest pain or pressure
  • confusion or drowsiness

*need to assess whole patient

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5
Q

what stage do you have if you are in 2 categories

A

choose the worse one

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6
Q

what are the causes of pre-renal AKI (volume responsive AKI) - 80%

A
  • caused by inadequate perfusion of kidneys
  • hypovolaemia eg. trauma, dehydration
  • loss of peripheral resistance eg. sepsis (slack blood vessels so decreased BP)
  • reduced cardiac output eg. heart failure
  • renovascular obstruction eg. thrombosis
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7
Q

how role do pharmacists play in preventing/managing pre-renal AKI

A
  • ensure hydration
  • manage sepsis by correct choice of antibiotics
  • optimisation of heart failure medicines
  • blood thinners/anti-platelets to prevent thrombosis
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8
Q

what are the causes of renal AKI (intrinsic AKI) - 10%

A
  • caused by any factor that causes damage either to kidney itself of the surrounding vasculature (inherited disorders, toxins etc)
  • Pre-glomerular - small arteries & arterioles e.g. wall disruption via malignant hypertension
  • Glomerular – glomerular capillary network e.g. glomerulonephritis
  • Post-glomerular - tubules & interstitium e.g. tubular necrosis
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9
Q

what are the causes of post-renal AKI (obstructive AKI) - 10%

A
  • involves obstruction of urinary outflow anywhere along the renal tract beyond the opening of the collecting ducts
  • Ureteric obstruction e.g. kidney stones
  • Bladder outflow obstruction e.g. benign prostatic hyperplasia
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10
Q

what are the risk factors for AKI (baseline risks)

A
  • advanced age
  • DM (high blood sugar so more pressure on kidneys to filter it)
  • CKD
  • heart failure as heart can’t pump as much blood
  • liver failure as decreased metabolism so more strain on kidneys
  • arterial disease (cholesterol build up in arteries)
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11
Q

what are the risk factors for AKI (clinical conditions) - reversible

A
  • sepsis
  • hypotension/shock
  • dehydration (most common, diuretics put you at risk)
  • rhabdomyolysis (destruction of striated muscle cells, toxic to kidney, SE of statins)
  • cardiac/vascular surgery (disturbs how much blood can be pumped)
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12
Q

complications of AKI

A
  • oliguria or anuria and oedema
  • hyperkalaemia
  • uraemia
  • hypertension
  • acidosis

CKD
- hyperphosphatemia
- anaemia
- hypocalcaemia

*bottom 3 are CKD

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13
Q

major role in primary prevention of AKI

A
  • recognise and assess high risk patients
  • assess fluid status/balance
  • obtain level of baseline renal function
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14
Q

role of clinical pharmacist in AKI prevention

A
  • appropriately manage nephrotoxic drugs
  • treat infections early
  • optimise the patients blood pressure
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15
Q

what is the pharmacists role in AKI

A
  • eliminate potential causes (e.g medicines with nephrotoxic potential)
  • avoid inappropriate combinations of medicines (ie - multiple BP medicines, would 1 do?)
  • ensure all medicines are clinically appropriate (due to renal function change)
  • if a medicine must be used:
  • Amend doses appropriate to renal function
  • Monitor blood levels of drug wherever possible (lithium, phenytoin, short therapeutic window)
  • Keep course as short as possible
  • following discharge, advise patient and GP which medicines have been stopped and if any need to be restarted
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16
Q

what medicines can cause AKI

A
  • NSAIDs/COX-II inhibitors
  • Diuretics
  • ACE inhibitors/ARBs
  • Iodine-based contrast media
17
Q

how do NSAIDs (aspirin, ibuprofen) cause AKI

A
  • inhibit synthesis of prostaglandins (COX pathway)
  • prostaglandins cause vasodilation of afferent arteriole
  • hence NSAIDs cause vasoconstriction
  • reduces renal blood flow and pressure in glomerular capillaries
  • reduces GFR
  • promotes fluid retention
18
Q

information about prostaglandins

A
  • PGI2, PGE1, PGE2 produced locally in kidney
  • vasodilatory agents so increase renal blood flow and GFR
  • released by dehydration, acute stress, SNS, angiotensin II
  • oppose vasoconstriction of SNS/angiotensinII (ie prevent excessive reduction in GFR and renal blood flow which can lead to renal ischaemia)
19
Q

when is NSAID use contraindicated

A
  • renal ischaemia
  • heamorrhagic shock
  • elderly
20
Q

how do ACE inhibitors/ARBs cause AKI

A
  • cause widening of the efferent arteriole (decreased vasoconstriction), which slows the renal blood flow, BP and reduces GFR
  • also get hyperkalaemia
  • Angiotensin receptor blockers prevent vasoconstriction and aldosterone release and hence same effects

*of importance in renal vascular disease, particularly those with bilateral renal artery stenoses, with reduced renal perfusion

21
Q

how do diuretics cause AKI

A
  • cause increased or excessive production of urine
  • hypovolaemia (loss of salt and water or a decrease in blood volume)
  • thus reducing renal blood flow
22
Q

how does iodine-contrast media cause AKI (taken for a scan, shows on screen)

A
  • causes contrast-induced nephropathy which is associated with a sharp decrease in kidney function over 48-72 hours
  • indicated by an increase in serum creatinine
23
Q

medicine sick day rules with AKI

A
  • unwell with:
    vomiting or diarrhoea - dehydration (unless minor)
    fevers, sweats, shaking
  • STOP taking these medicines and restart when well (after 24-48 hours or eating and drinking normally)
  • if in doubt contact pharmacist, GP or nurse
  • ACEIs (end in ‘pril’): lisinopril, perindopril, ramipril
  • ARBs (end in ‘sartan’):
    losartan, candesartan, valsartan
  • NSAIDs: (anti-inflam painkillers): ibuprofen, naproxen, diclofenac
  • diuretics: furosemide, spironolactone, indapamide, bendroflumethiazide
  • metformin (for diabetes)
24
Q

how would ACEI/ARB medication be affected by renal function

A
  • accumulate
  • lipid-lowering agents e.g. fibrates, statins
  • increased risk of rhabdomyolysis (toxic products)
  • stop if AKI due to rhabdomyolysis
  • otherwise, continue therapy but monitor
  • stop if patient develops unexplained / persistent muscle
25
Q

how would NSAID medication be affected by renal function

A
  • accumulate so avoid SR/XL preparations
  • increase in CNS side effects: drowsiness, confusion, respiratory depression
  • reduce dose and use short-acting where possible
  • use opiates with minimal renal excretion e.g. fentanyl, oxycodone, hydromorphone
26
Q

how would diuretic medication be affected by renal function

A
  • accumulate
  • hypokalaemia, hypocalcaemia, hypomagnesaemia, hyponatraemia, hyperuricaemia
  • tinnitus & deafness (usually with high doses and rapid IV administration)
  • overdiuresis leading to hypoperfusion of the kidneys can cause or exacerbate AKI
  • loop diuretics (furosemide & bumetanide) preferred as thiazides less effective if GFR < 25ml/min
  • however thiazides can potentiate the effects of loop diuretics
  • higher doses may be needed to achieve a diuresis in patients with fluid overload
  • monitor and adjust dose as necessary
  • potassium-sparing diuretics: if hypoperfusion of the kidneys, avoid
27
Q

how would metformin medication be affected by kidney function

A
  • renally excreted so avoid if GFR < 30ml/min
  • lactic acidosis - damage to vascular system and can end up in hypoglycaemia as can’t excrete metformin well
28
Q

what resource is used on wards for calculating kidney function

A

THINK kidney medicines optimisation tool

29
Q

what are the 2 main equations for calculating renal impairment

A
  1. Cockcroft and Gault (normally used due to variability)
  2. eGFR (MDRD)
30
Q

why is F lower for females in Cockcroft and Gault

A
  • F = location of fat/muscle
  • women store fat more densely on hips/breasts
31
Q

what is creatinine

A
  • product of muscle breakdown
  • depend how much muscle you have
  • entirely secreted by kidneys
  • 24 hour lag in secretion
32
Q

how do you calculate amputees renal function

A
  • what % of weight has been lost
  • consider in weight part of equation
33
Q

how do you calculate transgenders renal function

A
  • if on hormone treatment for 6 months or longer then kidneys will act as gender that you are transitioning to
  • if less than that then original gender
  • if won’t disclose – calculate by both methods and discuss with consultant for plan
34
Q

what are the problems when calculating renal impairment

A
  • may all have same Cr levels but doesn’t taken into consider weight/muscle mass
  • if frail, have little muscle mass and hence will need a reduction in dose
  • if a muscle builder, will have higher turnover of muscle and hence will need a increase in dose
  • if overweight, the excess weight doesn’t contribute to Cr but equation thinks so, so may need to use IBW
35
Q

what weight should we use with Cockcroft and Gault

A
  • ABW = Actual Body Weight (what you weigh)
  • IBW = Ideal Body Weight (what you “should weigh”)
  • DDW = Dose Determining Weight (IBW + a bit)
  • For obese patients, using ABW will over-estimate renal function potentially resulting in an overdose
  • No official guidelines on what to do, go by what place you work at recommends
  • A lot of places use a DDW
36
Q

what are the limitations with Cockcroft and Gault

A
  • extensive oedema (doesn’t contribute to Cr)
  • rapidly changing renal function
  • pregnant women (diff formula)
  • children (diff formula)
  • increased creatine consumption (supplements)
  • extremes of body mass
  • extremes of age
37
Q

what are the limitations with eGFR

A
  • very poor or good renal function
  • rapidly changing renal function
  • pregnant women
  • children
  • increased creatine consumption
  • extremes of body mass
  • age >75
  • doesn’t take into account patients size
    or weight (it standardises weight)
38
Q

when should you avoid nephrotoxic drugs

A
  • AKI
  • CKD 4-5
  • kidney transplants
  • ESRD: the damage is already done – drug choice is less important (but must still consider patient, side-effects, accumulation)
39
Q

what is the main source used in drug dosing in renal impairment

A

renal drug handbook (allows for more risk)

RENAL (13 decks)

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