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Year 3 - Script > Renal dysfunction > Flashcards

Renal dysfunction Flashcards

1
Q

How many deaths each year are associated with acute kidney injury

A

100,000 deaths each year

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2
Q

How many people who are 16 years and above have chronic kidney disease

A

6%

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3
Q

What does think kidneys campaign do

A
  • when to stop and re-start medicines
  • guidance on sick days
  • minimum data required to be communicated when a patient is discharged from hospital following an episode of AKI
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4
Q

Which drugs should not be given in kidney dysfunction

A
  • NSAIDs
  • strong opioids
  • indapamide - direutics can cause hypvolaemia whcih can cause AKI
  • amlodipine - not known to cause AKI but can cause hypotension and contribute to AKI
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5
Q

What are the three different classification of acute kidney injury

A
  1. Pre-renal
  2. renal
  3. post renal
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6
Q

Describe pre-renal AKI

A
  • reversible impairment of renal function from relative hypovolaemia or hypoperfusion
  • any condition reducing renal perfusion can potentially impair renal function
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7
Q

Describe renal AKI

A
  • damage within the kidney could result from more severe ischaemia, sepsis, inflammation or toxicity ( renal cells are sensitive to inflammatory or ischaemic injury)
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8
Q

Describe post renal AKI

A
  • Obstruction to urine outflow (e.g. enlarged prostate in men) causes a damaging back pressure within the kidney
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9
Q

Describe the 3 stages of severity of AKI

A

Stage 1

  • creatine rise of 26 micromol/litre or more within 48 hours or
  • creatine rise of greater than or equal to x 1.5 from baseline in 7 days or
  • reduced urne output of less than 0.5 ml/kg/hour for more than 6 hours

Stage 2

  • creatine rise of greater than and equal to x2 from the baseline or
  • reduced urine output of less than 0.5ml/kg/hour for 12 hours or more

stage 3

  • creatine rise of greater than or equal to x3 fro baseline within 7 days or
  • creatine rise to greater than or equal to 354 micromol/litre with either - acute rise in creatine of greater than or equal to 26 micromol/litre within 48 hours or a 50% rise from baseline within 7 days

or
- urine output of less than 0.3 ml/kg/hour for 24 hours
or
- anuria for 12 hours
or
- any requirement for renal replacement therapy

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10
Q

What should prescribing in AKI do

A
  • correct hypovolaemia
  • minimise renal hypoperfusion
  • treat other causes such as sepsis
  • avoid the use of (or withdraw) nephrotoxic agents
  • consider drugs that are renally excreted and may need adjustment
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11
Q

what drugs can induce nephrotoxicity

A
  • aminoglycosides
  • amphotericin
  • cytotoxic chemotherapy
  • diuretics
  • immunosuppressants
  • lithium salts
  • NSAIDs/COX-2 inhibitors
  • radiocontrast media
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12
Q

describe how aminoglycosides nephrotoxicity

A
  • they are directly nephrotoxic

- causes acute tubular necrosis

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13
Q

describe how amphotericin causes nephrotoxicity

A
  • directly nephrotoxic
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14
Q

Describe how cytotoxic chemotherapy can cause nephrotoxicity

A
  • e.g. cisplatin which has been associated with renal tubular damage
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15
Q

How does diuretics cause nephrotoxicity

A

lead to volume depletion

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16
Q

How do immunosuppressants cause nephrotoxicity

A
  • ciclosporin and tacrolimus cause renal vasoconstriction producing ischaemia
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17
Q

How do lithium salts cause neprhotoxicity

A
  • can cause tubulo-interstitial damage and chronic kidney disease with long term use
  • should only be suspended if there is known lithium overdose or toxic levels
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18
Q

How can NSAIDs/COX-2 inhibitors cause nephrotoxicity

A
  • renal blood flow often relies on prostaglandins

- NSAIDs and cycooxygenase-2 inhibitors reduce prostaglandin synthesis and cause renal hypoperfusion and AKI

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19
Q

How does radiocontrast media cause nephrotoxicity

A
  • high ionic load can produce renal vasoconstriction leading to ischaemia
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20
Q

Name some synthetic and naturally occurring agents that cause nephrotoxic

A

Synthetic agents

  • insecticides
  • herbicides

Naturally occurring agents

  • alkaloids from plants/fungi
  • reptile venoms
  • cocaine
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21
Q

Name pathological states that are nephrotoxic

A
  • hypoperfusion
  • sepsis
  • rhabdomyolysis
  • hepatorenal syndrome
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22
Q

describe the pathological states that are nephrotoxic

A
  • hypoperfusion = reduces oxygen and nutrient supply to the kidney
  • sepsis = endotoxins and inflammatory mediators from infection can damage the renal vascular endothelium resulting in thrombosis
  • rhabdomyolysis = myoglobin released from damaged muscles precipitates in renal tubules and also reduces blood flow in the outer medulla
  • hepatorenal syndrome = patients with end-stage liver disease often have renal vasoconstriction
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23
Q

What is the best indicator of function of the kidney

A
  • Glomerular filtration rate (GFR)
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24
Q

What is the eGFR derived from

A
  • CKD-EPI formula

- MDRD formula

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25
Q

In the UK what is the eGFR derived from

A

CKD-EPI

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26
Q

what is used as an estimate of eGFR

A
  • creatine clearance
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27
Q

What formula can be used to measure creatine clearance

A
  • The Cockcroft-Gault formula can be used to calculate estimated creatine clearance
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28
Q

when is the cockcroft-gault formula/creatine clearance used

A
  • estimating renal function or calculating drug doses in patients with renal impairment
  • older adults
  • patients at extremes of muscle mass
  • patients on a medicine with a low therapeutic index
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29
Q

if you are overweight …

A

eGFR is not an accurate reflection of the renal function

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30
Q

in what case do you not use the MDRD, CKD-EPI (or eGFR)

A
  • extremes of weight
  • children
  • pregnancy
  • catabolic states
  • reduced muscle mass - such as extreme old age, malnutrition, amputation and other muscle disorders
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31
Q

what can you use if you dont use the MDRD, CKD-EPI

A

= serum creatine

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32
Q

describe glomerular filtration

A
  • for filtration to occur the pressure within the capillary must be maintained at a fairly high level
  • the afferent enters the glomerulus and the efferent arteriole leaves the glomerulus
  • prostaglandins produced within the kidney maintain renal blood flow and GFR especially under conditions of reduced effective circulating volume
  • angiotensin II is produced by the renin angiotensin system in response to hypovolaemia or reduced renal perfusion
  • it causes effernet arteriolar vasoconstriction
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33
Q

what does inhibition of prostaglandin production do

A
  • inhibition of prostaglandin production or angiotensin II can compromise glomerular filtration and lead to AKI
34
Q

What are the stages of pharmacokinetics

A

ADME

  • absorption
  • distribution
  • metabolism
  • elimination
35
Q

Describe how renal impairment affects the pharmacokinetic stages

A
  • absorption = most drug absorption is unaffected by reduced renal function
  • distribution = protein binding of some drugs are affected in renal impairment
  • metabolism = some hepatic processes are affected by renal impairment but only at severe levels
  • elimination = water soluble drugs are particularly affected
36
Q

What happens to half life in renal impairment

A
  • half life is prolonged in renal impairment if the drug is significantly removed by the kidney
37
Q

what is the elimination half life

A
  • The elimination half life is the time taken for the plasma concentration of a drug to fall by half
38
Q

How can drug doses by adjusted in renal impairment

A
  • reducing the amount of the regular dose given

- extending the interval between regular doses (better for maintaining specific peak and trough concentrations)

39
Q

What is the ideal drug in renal impairment

A
  • no active metabolites
  • disposition unaffected by changes in fluid balance
  • disposition unaffected by changes in protein binding
  • pharmacodynamics unaffected by altered tissue sensitivity
  • a wide therapeutic window therefore safe as doses/serum concentrations increase
  • not inherently nephrotoxic
40
Q

what do you need to monitor in AKI

A

fluid balance

41
Q

How do you monitor patients in AKI

A
  • pulse - supine and upright
  • blood pressure - supine and upright
  • arterial oxygen saturation
42
Q

What should you do if you suspect hypovolaemia in AKI

A
  • check the supine heart rate and blood pressure

- a rise of heart rate on standing of more than or equal to 30 beats per minute

43
Q

What should you look for signs in AKI

A
  • pulmonary oedema - examine for tachypnoea, fine bilateral basal inspiratory crackles, chest x ray signs
  • fluid overload - check for pitting ankle and sacral oedema - check the patients weight daily
44
Q

What fluids should you prescribe in AKI

A
  • sodium chloride 0.9% is an appropriate IV fluid in AKI over 1 hour
  • sodium bicarbonate 1.26% is a good alternative if the patient has AKI with hypovolemia and a metabolic acidosis
45
Q

What are the two successive phases of AKI fluid replacement

A

Volume repletion

  • repeated fluid challenges with infusion of 250 to 500ml or more of sodium chloride 0.9% may best regimen
  • monitor vital signs, including urine output, in an acute or high dependency environment

Maintenance of fluid regimen

  • adjust prescribed regimens to take account of fluid balance if the patient requires continuing IV fluid therapy
  • reduce the rate of infusion so patient remains oliguric
46
Q

What should you be careful with fluid replacement

A
  • iatrogenic fluid overload risk pulmonary oedema and has recently been associated with increased mortality in AKI
  • reflex prescirbing of up to 3 to 4 litres of IV fluids per day wihtout proper fluid balance assessment is wrong and risks disaster
  • IV colloids do not provide any additional benefit for volume expansion and renal recovery compared with sodium chloride 0.9%
47
Q

What two parameters classify CKD

A
  • eGFR

- albumin:creatine ratio

48
Q

Name the stages of CKD

A
  • G1 - greater than 90
  • G2 - 60-90
  • G3a - 45-59
  • G3b - 30-44
  • G4 - 15-29
  • G5 - less than 15
49
Q

What is the most severe levels of CKD

A

G5

50
Q

who should you only use loop diuretic therapy in CKD

A
  • only consider diuretic therapy in fluid overload and or hyperkalaemia or hypertension in CKD
51
Q

What should you do for severe fluid overload requiring urgent treatment

A
  • use an infusion of a loop diuretic (e.g. up to 250mg of furosemide given neat via a syringe driver over 1 hour at a rate not exceeding 4mg/minute)
  • do not give bolus injections of loop diuretics - high infusion rates can cause deafness
  • infusions should be given with the benefit of specialist advice
52
Q

Why is combination diuretic regimes not recommended

A
  • intravascular volume depletion can occur rapidly and make renal dysfunction worse
53
Q

What diuretics should not be used with CKD

A
  • potassium sparing diuretics should not be used due to risk of hyperkalaemia
  • most thiazides are ineffective in severe renal impairment
  • metolazone does remain effective if the eGFR is less than 30ml/min/1.73m2 although it is associated with a risk of excessive diuresis - metolazone should only be inititiated under specialist supervision
54
Q

what two combination of medicines can reduce proteinuria

A
  • ACE inhibitors and spironolactone can reduce proteinuria
  • but the risk of hyperkalaemia with this combination means it should only be used on specialist advice in renal impairment
55
Q

what do you have to be careful of when prescribing ACE inhibitors to patients with CKD

A
  • serious hypotension can occur on initiation in susceptible patients with renal impairment - those prescribed high dose diuretic treatment for fluid overload are at particular risk due to dehydration and poor renal perfusion
56
Q

When prescribing ACE inhibitors with patients with CKD what should you do

A
  • monitor blood pressure closely

- carefully titrate the dose and monitor renal function

57
Q

What patients with CKD should you not use ACE inhibitors in

A
  • Bilateral renal stenosis
  • renal artery stenosis in a patient with a single functioning kidney
  • known wide spread vascular disease such as renovascular disease is likely to be present compromising blood flow
58
Q

describe how RAAS system causes rapid deterioration of renal function with AKI

A
  • RAAS system is stimulated in patients with poorly perfused kidneys
  • this produced angiotensin II which causes renal vasoconstriction in the efferent arterioles
  • this constriction of the outflow from the glomerulus creates a back pressure which maintains filtration at the glomerulus depsite overal poor kidney perfusion
  • blocking angiotensin II will lead to dilatation in efferent arterioles
  • leading to loss of back pressure and failure of filtration
59
Q

what is the target blood pressure for patients with

  • CKD
  • CKD and diabetes
A
  • CKD = 140/90mmHg

- CKD and diabetes and those with an ACR of greater than 70mg/mmol = 130/80mmHg

60
Q

How do you manage patients with hypertension

A
  • non drug therapy = important but unlikely to provide blood pressure control to target when used alone
  • Multiple antihypertensive agents = likely to be needed to provide BP control - this is particularly the case in hypertension owing to CKD
  • When ACE inhibitor/ARB therapy is used titrate this to the maximum tolerated dose before adding another agent
61
Q

Who should ACE/ARB inhibitors be offered to patients with CKD and..

A
  • diabetes mellitus and an ACR of 3 mg/mmol or more (ACR A2 or A3)
  • Hypertension and an ACE or 30 mg/mmol or more (ACE A3).
  • an ACR of 70 mg/mmol or more, irrespective of whether the patient is hypertensive or has cardiovascular disease
62
Q

What should you consider when prescribing ACE inhibitors/ARBs

A
  • avoid them in renovascular disease patients
  • avoid then in widespread vascular disease
  • check the potassium concentration and eGFR before treatment and 7 days later
  • do not start treatment if ACE.ARB is above the upper limit of normal - greater than 5 mmol/l
  • choose a cost effective ACE/ARB that allows once daily regimen
  • if the patients eGFR falls by 25% or more or serum creatinine increases by 30% or more at 7 day check look for other factors that may be causing the acute change, but if no others stop the ACE/ARB
  • if a dry cough causes problems with an ACE inhibitor switch to the ARB
63
Q

How can calcium channel blockers be used in hypertension in patients with CKD

A
  • agents are useful in CKD and hypertension

- they can produce oedema which is resistance to diuretics and can be confused with a volume overload

64
Q

How are diuretics used in patients with CKD and hypertension

A
  • crucial for blood pressure control in patients with salt and volume overload particularly in CKD stage G4/G5
  • and or when oedematous
65
Q

How are beta blockers used in patients with CKD and hypertension

A
  • have a limited role in hypertension management
  • now mainly used in resistant hypertension, hypertension accompanied by ischaemic heart disease or hypertension with heart fialure
  • use beta blockers such as bisoprolol or metoprolol as these have non renal elimination
  • start with a low dose and be aware of pharmacodynamic changes
66
Q

What beta blockers should you use in CKD

A

bisoprolol or metoprolol

67
Q

why is hyperkalaemia a particular problem in AKI

A
  • urinary excretion of potassium is reduced

- intracellular potassium may be released

68
Q

what causes an increase in extracellular potassium

A
  • rise rapidly following tissue damage such as burns, crash injuries, sepsis and ischaemia
69
Q

What increase the hyperkalaemia

A
  • hyperkalaemia is exacerbated by acidosis which causes potassium loss from cells
70
Q

what drugs affect potassium levels

A
  • Contain potassium = such as laxatives
  • act to retain potassium in serum = ACE inhibitors, ARBs, potassium sparing diuretics, NSAIDs
  • prevent intracellular buffering of potassium - beta blockers digoxin
71
Q

What drug should you stop straight away in uncontrolled hyperkalameia

A
  • ACE inhibitors and ARBs
72
Q

what level of potassium concentration should be treated straight away

A
  • Treat hyperkalaemia urgently if the serum potassium concentration reaches 6.5 mmol/k
73
Q

what are the aims of the treatment of hyperkalaemia

A
  1. protect the heart - stabilise the myocardium
  2. reduce the serum potassium concentration - drive potassium into the cells
  3. rid the body of excess potassium - stop the drugs contributing to hyperkalaemia and reduce potassium intake
74
Q

How do you protect the heart in hyperkalaemia

A
  • stablilise the heart with IV calcium gluconate 10%, 10-20ml (2.25-4.5) over 5-10 minutes
  • this stabilises the myocardium
  • protective effect begins in minutes but is short lived (less than 1 hour)
  • calcium chloride 10% in 10ml syringes provides 6.8 mmol of calcium is given by slow intravenous injection
75
Q

Name two drugs that can be used to reduce serum potassium concentration

A
  • nebulised salbutamol

- soluble insulin

76
Q

describe nebulised salbutamol reduces serum potassium concentration

A
  • glucose drive potassium into the cells
  • in those patients where an effect is obtained it will reduce serum potassium by up to 1mmol/l and last for 2 hours
  • not effective for all patients and will not lower the potassium permanently
  • it is to be seen as a temporary emergency measure if used
77
Q

describe how soluble insulin reduces serum potassium concentration

A
  • 50ml of 50% glucose together with 5-10 units of soluble insulin over 10 minutes
  • insulin promotes intracellular potassium uptake so reducing serum levels
  • the effect becomes apparent after 15-30 minutes and peaks after about 1 hour and lasts for 2-3 hours
  • it will decrease potassium by around 1mmol/l
  • omit exogenous glucose if the serum glucose is more than 15mmol/l
  • monitor the glucose after 30 minutes then hourly for 6 hours to check for delayed hypoglycaemia which is a common problem - the hypoglycemia effects lasts longer than the potassium lowering effect
78
Q

What drugs should you stop that promote hyperkalaemia in hyperkalameia

A
  • ACE inhibitors
  • ARBs
  • NSAIDS
  • oral potassium supplements
  • potassium-sparing diuretics
  • metformin - risk of lactic acidosis
79
Q

How do you correct the metabolic acidosis that develops in hyperkalaemia

A
  • in CKD - correct acidosis with oral sodium bicarbonate 1-6g day in divided doses
  • in AKI correct acidosis with 50-100mmol of IV bicarbonate ions - 1.4 to 1.26%,2 50-500mls over 15 to 60 minutes
  • do not mix bicarboante and calcium in the same line as an insoluble precipitate will form
  • bicarbonate activates the cell membrane Na/H exchanger producing an increase in intracellular sodium which promotes increased activity of Na-K-ATPase resulting in increased intracellular sequestration of potassium
  • if the patient is fluid overload, IV sodium bicarbonate can exacerbate this - in this case dialysis may be the only viable action
80
Q

What drug do you use to restrict dietary potassium

A
  • calcium polystyrene sulphonate - 15-30g two to four times a day
81
Q

How does calcium polystyrene sulphonate work

A
  • the ion exchange resin binds potassium in the GI tract releasing calcium in exchange, thus physically removing potassium from the body
  • give it in conjunction with lactulose to reduce the risk of faecal impaction
  • monitor potassium closely especially as the therapeutic effect of calcium resoium can continue to work for some time even after treatment has stopped
82
Q

What are the signs of hyperkalaemia in an ECG

A
  • loss of P waves
  • Prolonged PR interval
  • QRS widening

Year 3 - Script (11 decks)

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