Week 4 - C - Acute kidney injury and Chronic kidney disease Flashcards

1
Q

Acute kidney injury may be due to pre renal, intrinsic renal or post renal causes What was acute kindey injury previously known as?

A

Acute kidney injury was previously known as acute renal failure

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2
Q

What is acute injury defined as?

A

o Acute kidney injury is defined as a rapid reduction in renal function over hours/days, as measured by serum urea and creatinine – leading to failure to maintain fluid, electrolyte and acid-base homeostasis

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3
Q

What is the measured blood creatinine in acute kidney injury for diagnosis? What happens to the urine output in acute kidney injury?

A

blood creatinine level has risen from the baseline value for that person (by 26 micromoles per litre or more within 48 hours)

blood creatinine level has risen over time (by 50% or more within the past 7 days)

The urine output greatly decreses in acute kidney injury

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4
Q

• Pre-renal are those which reduce renal perfusion – this is the most common cause (40-70%) Give some example causes? (give some non drug examples which can cause the renal hypoperfusion)

A

They include major haemorrhage, hypovolaemia due to severe diarrhoea, reduced renal perfusion associated with severe sepsis, and hypotension due to cardiac causes eg. Myocardial infarction

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5
Q

Renal hypoperfusion is especially worse in patients with renal artery stenosis How is renal artery stenosis diagnosed? What is heard on ausculatation during a renal examination?

A

Renal artery stenosis is diagnosed by US for blood flow to the kidneys

But gold standard is by carrying out CT angiogram

Listen for renal bruits on auscultation suggesting turbulent blood flow due to the stenosis

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6
Q

Still on pre renal causes of acute kidney injury, what drugs are contraindicated? And which is contrainidcated in bilateral renal artery stenosis?

A

Do not give NSAIDs as this constricts the afferent arteriole and this could lead to even more underperfusion

Do not give ACEI/ARBs in renal artery stenosis -

o Due to reduced ATII so efferent arteriolar vasodilation - fall in GFR - increased serum creatinine

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7
Q

o If renal perfusion is restored in time, renal function recovers quickly – it is reversible If renal function is not restored, what will happen?

A

Patient will undergo inrtinsic failure due to acute tubular necrosis

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8
Q

What are the two main causes of acute tubular necorisis?

A

A low blood pressure causing prolonged renal hypoperfusion and nephrotoxic drugs

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9
Q

What type of cast are basically always showing acute tubular necrosis?

A

Muddy brown casts

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10
Q

Give an example of a nephrotoxic drug?

A

Gentamicin

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11
Q

What are two other causes of intrinsic actue kidney injury?

A

Can have glomerulonephritis and acute interstitial nephritis

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12
Q

destruction of large volume of skeletal muscle causing myoglobin protein to be present in renal tubules – toxic! What is this condition?

A

Rhabdomyolysis

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13
Q

Post-renal AKI is due to obstruction of the urinary tract. If the patient previously had normal renal function, and has 2 kidneys, both must be obstructed to cause AKI Where must the obstuction be to cause AKI if post renal?

A

Obstruction present in the bladder or urthra to cause bilateral AKI

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14
Q

What is the treatment of post-renal AKI?

A

Catheter - can go with nephrostomy

(artificial opening between kindey and skin to drain urine)

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15
Q

NSAIDs as stated can cause intrinisc kidney injury they cause vasocontriction of the affterent arteriole Are NSAIDs linked to glomerulonephritis or intersitital nephritis? Whcih other drugs cause it?

A

They are linked to interstitial nephritis

Also caused by PPIs

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16
Q

Acute kidney injury can lead to a patient entering hyperkalaemia as the kidney fails to secrete acid and therefore tries to compensate What is the treatment for hyperkalaemia? urgent treatment

A

Give 10ml calcium gluconate 10% intravenously.

This doesn’t lower serum potassium, but protects the heart against arrhythmias.

Give 10 units Actrapid insulin with 50ml glucose 50% intravenously.

Insulin causes potassium to move into cells.

Glucose must be given with insulin to prevent hypoglycaemia, and blood glucose level monitored.

Give 10mg salbutamol by nebuliser. β-agonists also cause potassium to enter cells.

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17
Q

What type of action is the insulin analogue ActRapid? What is the chemical name for act rapid?

A

This is a short acting insulin action

Chemical name = soluble insulin

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18
Q

Give the brand name of 2 rapid acting insulin analogues?

A

Novorapid and humalog

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19
Q

WHat is the chemical name for Novorapid? What is the chemical name for humalog?

A

Novorapid - insulin aspart

Humalog - insulin lispro

20
Q

What is the brand name for insulin glargine? What is its type of action?

A

Brand name - Lantus

Type of action - long acting

21
Q

Give the chemical and brand name of 2 rapid and short acting insulin drugs Give the chemical and brand name of one long acting?

A
  • Rapid -
    • Insulin lispro- Humalog
    • Insulin aspart - Novorapid
  • Short -
    • Soluble insulin - ActRapid or
    • Humulin S
  • Long acting - Insulin glargine - Lantus
22
Q

For meals, usually a rapid acting insulin is given and a long acting is given at the start of the day This is the basal bolus regime Name the options for the basal dose and the bolus doses? Bolus is given with meals

A

Basal dose - long acting -

  • Insulin glargine - Lantus

Bolus dose - rapid acting -

  • Insulin aspart - Novorapid
  • Insulin lispro - Humalog
23
Q

What would the ECG show in signs of hyperkalaemia?

A

Peaked or ‘tall-tented’ T waves (occurs first)

Loss of P waves

Broad QRS complexes

Sinusoidal wave pattern

Ventricular fibrillation

There would be associated muscle weakness also

24
Q

In acute kidney injury, why can a person enter hyperkalaemia?

A

The kidney is failing to secrete acid and this is leading to a build up of acid in the blood causing a metabolic acidosis

The kdiney therefore tries to exchange potassium for hydrogen ions to fix the matabolic acidosis

Check ECG and bloods for life threatening hyperkalaemia

25
Q

In hyperkalaemia, none of the measures actively remove potassium from the body so what is likely to be required?

A

Haemodialysyis is likely to be required

26
Q

Arrange an ultrasound scan of the kidneys if suspected AKI. Ultrasound is needed (1) to check for obstruction (2) to check the size of the kidneys What will the size of the kidneys tell you about in chronic kidney disease vs acute kidney injury?

A

In chronic kidney disease the kidneys would have been scarred and therefore become atrophic so on ultrasound it will look small

27
Q

What is the prevalence of chronic kidney disease? (what percentage of the population is affected)

A

Approximately 11% of the population is affected

28
Q

There a 5 stages of chronic kidney disease with different eGFR values for each stage What are the eGFR values for each stage?

A

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29
Q

Which stages of chronic kidney disease is evidence of kidney damage required? What kind of evidence could this be?

A

Stages 1 and 2 Stage 1 - eGFR normal/ >90 Stage 2 - eGFR 60-90 This evidence may be proteinuria, or abnormalities on scanning.

30
Q

Examples: A patient with polycystic kidneys, identified on ultrasound, with a GFR of 100ml/min, would have which stage of CKD?

A

This would be stage 1 CKD

31
Q

A patient with scarring seen on ultrasound, caused by reflux nephropathy, and a GFR of 66ml/min, would have which stage of CKD?

A

Stage 2 CKD

32
Q

A patient with hypertension, proteinuria 1.2G/day, and a GFR of 78ml/min, would have which stage of CKD?

A

This would again be stage 2 CKD

33
Q

An 82 year old lady with a GFR of 76ml/min, normal urinalysis and a normal ultrasound scan, would have which stage of CKD?

A

This patient would not have CKD as they have no evidence of kidney damage

34
Q

After the age of 40, GFR declines by about 0.75ml/min/yr Which stages are defined by GFR values alone?

A

This would be stages 3-5

35
Q

Note that mild to moderate (Stages 1-3) CKD is common, whereas severe (stages 4-5) CKD is not. It is clear from this that most patients with early CKD DO NOT PROGRESS to advanced CKD, and never need dialysis or a renal transplant. However, almost all patients who are on dialysis did at some time have early CKD

Why is stage 3 CKD important?

A

This is because it increases the risk of cardiovascular mortality

36
Q

Patients do not suffer from symptoms due to reduced GFR until the GFR Is very low Usually below what levels before they begin to suffer from symptoms?

A

Usually a GFR below 20ml/min

37
Q

When suspecting CKD in practice What tests is carried out initially?

A

Carry out urinalysis

38
Q

proteinuria increases the risk of progression of CKD; haematuria may indicate renal disease or a lesion of the lower urinary tract

If proteinuria is present, what must be carried out to quantify the amount?

A

Carry out either a 24hour protein output or Protein: creatinine ratio test

39
Q

Can chronic kidney disease be diagnosed from one urine creatinine measurement? When may creatinine go up or down physiologically and therefore is not reliable as an indicator of renal function?

A

Needs multiple emasurememnts over a long period of time

Creatinine may go up or down physiologically

Up - very muscular perosn

Down - decreases with age as GFR decreases by about 0.75ml/min/year

40
Q

What is a complication of CKD in regards to red blood cell count and how?

A

Can lead to renal anaemia

Kidneys produce erythropoetin which causes the bone marrow to begin erythropoeisis (RBC production)

Therefore if the kidneys are damaged this will cause anaemic

41
Q

What is a complication of CKD in regards to bone disease and how? What type of hyperparathyroidism is this describing?

A

IF the kidneys ar not working they canot convert calcidiol (25OHVitamin D3) to calcitriol (1,25, diOH vitamin D3)

Therefore calcium is not absorbed from the intestines leading to an increased PTH in response to the hypocalcaemia, this causes increased bone resoprtion causing hyperphosphataemia and increasing the calcium

CKD leads to secondary hypeparathyroidism

42
Q

Stage 3 CKD with urine PCR >100mg/mmol Stage 3 CKD with progression (GFR falling by >20% over 6 months) Stage 3 CKD in younger people (age 100mg/mmol mean

A

Nephrotic syndrome

Protein:creatinine ratio >100mg/mmol

43
Q

What is the primary option for treatment of end sage renal failure?

A

Renal replacement therapy - transplant if able

Dialysis if not

44
Q

What groups of people are more likely to have chronic kidney failure?

A

Those with diabetes, hypertension, glomerulonephritis, reflux nephropathy, polycystic kidneys

45
Q

What are the symptoms of chronic kidney disease? Usually arise very late

A

These would be tirendess, poor appetite and itchy

46
Q

 Slow progression, reduce cardiovascular risk, identify and treat complications of CKD, and prepare for renal replacement therapy Which drugs will reduce the blood pressure and the proteinuria in CKD?

A

• ACEI and ARBs reduce BP and proteinuria, also evidence for spironolactone

47
Q

What may there be an initial change in when giving ACEinhibtors and is therefore important to monitor?

A

There may be an initial decrease in GFR due to the ACEI/ARBS causing vasodilation of the afferent arteriole

May also be hyperkalaemia - the decreased GFR will mean more acid meaning potassium isnt secreted