Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal and Urology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

definition

A

abrupt reduction in renal function (over a period of less than 48 hours) defined as
- absolute increase in creatinine above 26.4micromol/litre
OR
- increase in creatinine by 50% or more
OR
- reduction in urine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

the term acute kidney injury can only be used when

A

adequate fluid resuscitation has been attempted and an obstruction has been ruled out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

KDIGO STAGING CLASSIFICATION stage 1

A
  • increase in creatinine above 26micromol/litre or increase in creatine above 1.5-1.9x reference creatinine
  • urine output less than 0.5ml/kg/hour for more than 6 consecutive hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

KDIGO STAGING CLASSIFICATION stage 2

A
  • increases in creatinine above 2 to 2.9x reference value

- urine output less than 0.5ml/kg/hour for more than 12 consecutive hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

KDIGO STAGING CLASSIFICATION stage 3

A
  • increase in creatinine greater than 3x reference value

- urine output less than 0.3ml/kg/hour for 24 hours or 12 hours for aneuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Risk factors for acute kidney injury in the patient

A
  • older age
  • previous AKI
  • chronic kidney disease
  • diabetes
  • heart failure
  • liver disease
  • PVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Exposure risk factors for acute kidney injury

A
  • hypotension
  • hypovolaemia
  • sepsis
  • deteriorating NEWS
  • recent contrast
  • exposure to certain nephrotoxic medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of AKI are divided into 3

A
  • pre- renal causes (functional)
  • renal causes (structural)
  • post-renal causes (obstructive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pre-renal acute kidney injury caused by

A

decreased blood flow to the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pre-renal AKI can be due to

A
  • absolute loss of body fluid
  • relative loss of fluid
  • renal hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

absolute loss of body fluid caused by

A

fluid actually leaving the body caused by haemorrhage, diarrhoea and vomiting or burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

relative loss of body fluid caused by

A

total amount of fluid within the body stays the same

  • distributive shock= fluid moves from within blood vessels into the tissues
  • cariogenic shock= seen in congestive heart failure where there is impaired pumping of the heart so blood pools in the venous side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

renal hypo perfusion is caused by

A

problem localised to the renal artery

  • renal artery stenosis
  • hepato-renal syndrome
  • NSAIDS, cox-2 inhibitors, ACE inhibitors and ARBS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

in all of the causes of pre-renal AKI

A

there is reduced blood flowing to the glomerulus therefore, there is a reduction in glomerular filtration rate therefore, reduced amount of creatinine and urea get filtered which causes azotemia and also causes oliguria §

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

oliguria

A

less than 0.5mls/kg/hour of urine is produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

normal urine output

A

0.5mls/kg/hour which amounts to 30mls/ hour in a 60kg person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

less blood getting filtered through the kidney also activates what

A

the RAAS system which causes the release of aldosterone by the adrenal cortext which causes the kidneys to re-asbord sodium and water which causes the re-absorption of even more urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

the re-absorption of sodium and water means that

A

less sodium is excited and because less water is excreted urine becomes very concentrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

in pre-renal AKI urine osmolarity

A

is greater than 500mosmol/kg most of which is urea which is why the urine smells so strongly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ACE inhibitors reduce production of what

A

angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

function of angiotensin II

A

mediates arterial vasoconstriction which increased glomerular filtration rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ACE inhibits can cause

A

a fall in glomerular filtration rate by causing efferent arteriolar vasodilation therefore, someone on an ACE inhibitor should stop it if they get diarrhoea or vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

untreated pre-renal AKI will cause

A

acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

acute tubular necrosis

A

hypo perfusion to the renal tubular cells causes ischaemia, infraction and necrosis of the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

common causes of acute tubular necrosis

A

sepsis, severe dehydration, rhabdomyolysis and drug toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

acute tubular necrosis is the most common cause of what

A

acute kidney injury in hospital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

treatment of pre-renal AKI

A
  • Assess for hydration= blood pressure, heart rate, urine output, JVP, capillary refill time, oedema
    If hypovolaemia= crystalloid fluids (0.9% NaCl) give 500mls and repeat as required or colloid (gelofusin)
  • if you have given 1 litre and still no improvement get help!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

renal AKI is caused by

A

an damage to the glomerulus, tubules or intersitium

29
Q

tubular causes

A
  • most common cause is acute tubular necrosis
30
Q

acute tubular necrosis commonly occurs

A

because of a pre-renal AKI and can also be caused by nephrotoxins

31
Q

nephrotoxins include

A

amino glycoside (gentamicin), lead, myoglobin released in rhabdomyolysis, ethylene-glycol (anti-freeze), radio-contrast dye, uric acid

32
Q

uric acid is a

A

waste product that can build up during chemotherapy called tumour lysis syndrome

33
Q

whatver the cause of acute tubular necrosis when the cell die off

A

they slough off and block the renal tubule increasing the pressure within the tubules, so fluid is trying to flow from the high pressure glomerulus into the high pressure glomerulus which just does not work therefore, glomerular filtration rate falls causing azotema and oliguria

34
Q

necrotic tubular cells cannot participate in what

A

re-absoprtion or secretion which cause potassium to build up causing hyperkalaemia and a build up of hydrogen ions causing a metabolic acidosis

35
Q

acute tubular necrosis causes a

A

brown granular cast

36
Q

if the underlying cause of the acute tubular necrosis is addressed then

A

people can recover because the tubular cells can regenerate over the course of a few weeks

37
Q

what is another cause of renal AKI

A

GLOMERULONEPHRITIS

38
Q

glomerulonephritis is often caused by

A

antigen-antibody complexes deposition in the glomerular tissue which activates the complement system which attracts macrophages and neutrophils which then release lysosomal enzymes causing inflammation and damage to the podocytes which causes proteinuria and haematuria because large molecules can enter the filtrate

39
Q

also the fluid leakage in glomerulonephritis causes a

A

reduction in the pressure difference which drives filtration of small molecules causing a reduction in GFR causing oliguria and more fluid remains in the blood causing oedema and hypertension

40
Q

in glomerulonephritis the inability to excrete nitrogenous waste products causes

A

azotemia

41
Q

another cause of renal AKI is

A

acute interstitial nephritis

42
Q

acute interstitial nephritis

A

inflammation of the interstitial over the course of a few days-weeks
this inflammation is caused by the infiltration of immune cells (neutrophils and eosinophils)

43
Q

acute interstitial nephritis is typically caused by

A

NSAIDS, penicillins and diuretics

44
Q

early symptoms of acute interstitial nephritis

A

oliguria and eosinophiluria and fever and a rash

45
Q

symptoms of acute interstitial nephritis

A

usually resolve is the medication is stopped but if not it will cause renal papillary necrosis which causes haematuria and loin pain

46
Q

initial investigations for AKI

A
  • Us+Es= Na, K, urea and creatinine
  • FBCS and coagulation screen
  • urinalysis
  • ultrasound
  • immunology= ANA, ANCA and GBM
  • protein electorpheres and bens jones protein if there is a suspicion of myeloma
47
Q

indications for renal biopsy

A
  • urgent indications= suspected rapidly progressive GN, positive immunology and AKI
  • semi-urgent indications= unexplained AKI requiring diagnosis, rule out obstruction and volume depletion
48
Q

before renal biopsy you must ensure

A

it is safe to carry out

- normal clotting, normotensive and no hydronephrosis

49
Q

post-renal AKI

A

caused by obstruction of outflow from the kidneys

50
Q

post- renal AKI caused by

A
  • external compression of the ureters (intra-abdominal tumour of urethra (benign prostatic hyperplasia)
  • internal blockage (kidney stones, strictures, cancer)
51
Q

if only 1 ureter is obstructed

A

called a unilateral obstruction and if the other kidney is functioning normally then kidney function is normal preserved

52
Q

if both ureters are obstructed or the uretrha is obstructed

A

called a bilateral obstruction and this causes post-renal AKI

53
Q

whatever the cause of obstruction it will cause

A

backlog of fluid into the kidney into the renal tubules causing an increase in pressure within the renal tubules therefore, reducing the glomerular filtration rate

54
Q

reduction in GFR means

A

less creatinine and urea will get filtered causing azotemia and also causes oliguria

55
Q

high pressure within the renal tubule initially increase the

A

re-absorpton of sodium, water and urea

56
Q

but over time the increased pressure within the renal tubules causes

A

the epithelial cells within the tubules to get damaged which are the cells responsible for re-absorpton so less sodium and urea get re-absorebed

57
Q

management of post-renal AKI

A

catheter and if this fails a nephrostomy

58
Q

life-threatening complications of AKI

A
  • HYPERKALAEMIA
  • FLUID OVERLOAD
  • SEVERE METABOLIC ACIDOSIS (PH LESS THAN 7.15)
  • uraemia pericardial effusion
  • server uraemia (urea greater than 40)
59
Q

normal potassium is between

A

3.5-5

60
Q

hyperkalaemia

A

potassium greater than 5.5

61
Q

life-threatening hyperkalaemia

A

potassium greater than 6.5

62
Q

hyperkalaemia causes

A

muscle weakness and cardiac arrhythmias

63
Q

ECG changes in hyperkalaemia

A 
K=6-7= Peaked T waves
K= 7-8= flatted p waves, prolonged PR interval, depressed ST segment and peaked T wave
K= 8-9= atrial standtil, prolonged QRS duration
K= greater than 9= sine-wave pattern
64
Q

management of hyperkalaemai

A
  • cardiac monitoring and IV access
  • 10ml 10% calcium glutinate (OVER 2-3 minutes)
  • Insulin (10 units act rapid) with 50mls 50% dextrose (over 30 minutes)
  • salbutamol nebulised (over 90 minutes)
65
Q

calcium gluconate

A

does not actually affect potassium levels but it reduces the excitability of cardiomyoctes reducing the risk of ventricular fibrillation

66
Q

insulin

A

facilitates the uptake of glucose into cell causing intra-cellular shift in potassium

67
Q

salbutamol

A

promotes cellular uptake of potassium

68
Q

drugs causing hyperkalaemia

A

spironolactone, ramipril, atenolol and amiloride (potassium sparing diuretic)

69
Q

indication for urgent haemodialysis

A
  • hyperkalaemia (any potassium greater than 7 or greater than 6.5 with no repose to medical management)
  • severe acidosis pH less than 7.15
  • fluid overload
  • urea great than 40 or pericardial rub or effusion

Renal and Urology (51 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions