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URINARY > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

what are the 6 main functions the kidneys

A
  1. body fluid homeostasis
  2. regulation of vascular tone
  3. excretory function
  4. electrolyte homeostasis
  5. acid-base balance
  6. endocrine function
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2
Q

what is the traditional definition of acute renal failure

A

rapid loss of glomerular filtration ad tubular function over hours to days

retention of urea/creatinine

oliguric/non-oliguric

potentially recoverable

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3
Q

what is the relationship between serum creatinine and GFR

A

as % normal GFR falls, serum creatinine levels rise
BUT
creatinine levels will only start to rise after loss of 60% of normal GFR

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4
Q

what is the current definition of acute kidney disease (i.e. include specific values)

A

an increase in serum creatinine:

  1. by >26.5 micro mol/l within 48hrs
    OR
  2. to >1.5 times baseline - which is known or presumed to have occurred within the prior 7 days

Urine volume <0.5 ml/kg/h for 6 hours

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5
Q

what are the serum creatinine levels and urine output for stage 1 acute kidney injury

A

SC:
1.5–1.9 times baseline
OR ≥ 26.5 μmol/l increase

URINE:
<0.5 ml/kg/h for 6–12 hours

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6
Q

what are the serum creatinine levels and urine output for stage 2 acute kidney injury

A

SC:
2.0–2.9 times baseline

URINE:
<0.5 ml/kg/h for ≥12 hours

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7
Q

what are the serum creatinine levels and urine output for stage 3 acute kidney injury

A

SC:
3.0 times baseline
OR Increase to ≥354 μmol/l (and above)
OR Initiation of renal replacement therapy

URINE:
<0.3 ml/kg/h for ≥ 24 hours OR Anuria for ≥12 hours

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8
Q

how many hospital admissions are complicated by AKI

A

1 in 5-7

more than half in ITU admissions

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9
Q

what are the immediate consequences of AKI

think vowels - AEIOU

A 
A - acidosis
E - electrolyte imbalance 
I - Intoxication TOXINS
O - overload
U - Uraemic complications
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10
Q

explain how each of the immediate dangerous consequences come about (AEIOU)

A

A - not reabsorbing bicarbonate - blood pH goes down = cardiac arrest

E - not reabsorbing or reabsorbing too many electrolytes - can lead to e.g. hyperkalaemia = cardiac arrest

I - toxin build up (e.g. opiates) due to not being removed from kidneys = respiratory (and then cardiac) arrest

O - fluid not being removed - fluid and pulmonary oedema = cardiac arrest

U - urea in the blood = renal failure

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11
Q

what are the three groups of causes for AKI

A

pre-renal
- blood flow to kidney

renal (intrinsic)
- damage to renal parenchyma

post-renal
- obstruction to urine exit

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12
Q

what are the 3 types pre-renal causes

A
  1. reduce effective circulation volume:
    - sepsis
    - hypovolaemia (haemorrhage, burns,
    vomiting/diarrhoea, diuretics)
    - hypotension (medications)
    - cardiac failure
  2. arterial occlusion
  3. vasomotor
    - NSAIDS/ACE inhibitors
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13
Q

what are the 6 types of renal (intrinsic) causes

A
  1. acute tubular necrosis (ATN)
    - ischaemia
  2. toxin related
    - drugs
    - radiocontrast
    - rhabdomyolysis (Haem pigments)
    - snake venom, heavy metals, mushrooms, etc
  3. acute interstitial nephritis
  4. acute glomerulonephritis
  5. myeloma
  6. intra renal vascular obstruction
    - vasculitic
    - thrombotic microangiopathy
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14
Q

what is rhabdomyolysis

A

when there is break down of muscle (e.g. crushing injury) and the break down products go to get filtered at the kidneys but can’t - lead to build up of toxic breakdown products

**included are harm pigments from blood so on dipstick would show blood in urine BUT under microscope would NOT show blood cells

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15
Q

what is the post-renal cause

A

obstruction

  • intraluminal (calculus, clot, sloughed papilla)
  • intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
  • Extramural (retroperitoneal fibrosis, malignancy)
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16
Q

can different groups of causes occur simultaneously

A

yes - often several causes co-exist i.e. can have pre and intrinsic causes

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17
Q

what is the most common cause of AKI

A

poor perfusion leading to established tubule damage

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18
Q

what is ischaemic renal injury

A

tubular necrosis

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19
Q

what occurs in the initiation stage of ischaemic renal injury

A

exposure to toxic/ischaemic insult

renal parenchymal injury evolving

AKI potential preventable at this stage

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20
Q

what occurs at the maintenance stage of ischaemic renal injury

A

established parenchymal injury

usually maximally oliguric now

typical duration 1-2 weeks (but can be up to several months recovery)

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21
Q

what occurs at the recovery stage of ischaemic renal injury

A

gradual increase in urine output

fall in serum creatinine (may lag behind diuresis)

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22
Q

what happens if GFR recovers quicker than tubule restive capacity

A

excessive diuresis - eg ost obstructive natriuresis

23
Q

what is radio contrast nephropathy

A

AKI following administration of iodinated contrast agent

usually transient renal dysfunction that resolves after 72hrs
BUT
may lead to permanent loss of function

24
Q

what are risk factors for radio contrast nephropathy

A 
Diabetes mellitus
Renovascular disease
Impaired renal function
Paraprotein
High volume of radiocontrast
25
Q

what is myeloma

A

A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains

26
Q

what are the clinical signs of myeloma

A 
Anaemia
Back pain
Weight loss
Fractures
Infections
Cord compression
Markedly elevated ESR
Hypercalcaemia
27
Q

how can myeloma be diagnosed

A

Bone marrow aspirate - >10% clonal plasma cells

Serum paraprotein ± immunoparesis

Urinary Bence-Jones protein (BJP)

Skeletal survey - lytic lesions

28
Q

what are the types of renal failure associated with myeloma

A

Cast nephropathy - ‘myeloma kidney’

Light chain nephropathy

Amyloidosis

Hypercalcaemia

Hyperuricaemia

29
Q

SUMMARISE: what are the causes of AKI

A

pre

  • cardiac failure
  • haemorhage
  • sepsis
  • vomiting/diarrhoea

renal (intrinsic)

  • glomerulonephritis
  • vasculitis
  • radiocontrast
  • myeloma
  • rhabdomyolisis
  • drugs (NSAIDS, gentamicin)

post

  • tumours
  • prostate disease
  • stones
30
Q

what investigations assessments would you do for AKI

A
  • Renal function etc
  • Urine dipstick
  • FBC
  • USS
  • Blood gas
  • renal biopsy
  • history
  • examination - vital signs, fluid status, systemic illness, etc
  • drugs
  • insults
31
Q

how can AKI be prevented

A
  • avoid dehydration
  • avoid nephrotoxic drugs/toxins
  • treat sepsis
  • hold medication
  • give fluids - optimise BP and volume status

**review clinical status of those at risk

32
Q

what does the STOP AKI acronym stand for

A

how to prevent AKI

S - treat Sepsis
T - Toxins
O - Optimise BP
P - Prevent harm

33
Q

what is the main focus of management for AKI

A

remove/treat if possible

pre - do they need fluid? BP support?

renal - can you remove precipitant?

post - do they need catheter?

34
Q

what does supportive management of AKI involve

A

fluid balance

  • volume resuscitation if depleted
  • fluid restriction of overload

optimise BP

  • give fluid/vasopressors
  • stop ACE inhibitors/ antihypertensives

stop nephrotoxic drugs

  • NSAIDs
  • aminoglycosides
35
Q

what are the 5 Rs for IV prescribing

A
  1. Resuscitation - IV fluids to restore circulation
  2. Routine maintenance - IV fluids if can’t take maintenance requirements orally/enterally
  3. Replacement - not resuscitation but IV ADDITIONAL to correct existing deficit or abnormal EXTERNAL losses e.g. vomiting
  4. Redistribution - IV fluids for abnormal INTERNAL fluid redistribution eg oedema
  5. REASSESSMENT
36
Q

what is the normal fluid intake/output

A

2500ml in

2100-2600ml out

37
Q

how would you remove the precipitant of AKI

A

stop drugs that are causing

treat sepsis

diangnose GN/other interstitial disease and give specific therapy

38
Q

how can you stop AKI getting worse

A

support BP

  • vasopressors
  • stop antihypertensives

reduce further insults - e.g. don’t give IV radio contrast unless needed

39
Q

what are the ECG changes in hyperkalaemia

A

earliest sign = peaked T waves (tall tented T waves

P waves widen and flatten

PR sement lengthens

P waves eventually disappear

QRS intervals prolonged

Sinus bradycardia or slow AF

asystole
ventricular fibrillation

**depolarisation less marked - repolarisation more marked

40
Q

what can hyperkalaemia ultimately lead to

A

cardiac arrest

41
Q

what are the 3 stages of hyperkalaemia treatment

A

stabilise (myocardium)
- calcium gluconate

shift (K+ intracellularly)

  • salbutamol
  • insulin-dextrose

remove

  • diuresis
  • dialysis
  • anion exchange resins
42
Q

how is intoxication treated

A

use antidote if available

  • morphine = naloxone
  • digoxin - digibind

may require RRT

43
Q

what are the indications for dialysis in acidosis

A

**decreased HCO3-

increased lactate

increased pCO2

44
Q

what are the indications for dialysis in electrolyte imbalance

A

**increased K+

increased OR decreased Na+

increased Ca2+

increased uric acid

increased PO4-

increased Mg2+

45
Q

what are the indications for dialysis in intoxication/toxins

A

Aspirin

theophylline

lithium

ethylene glycol

methanol

metformin

46
Q

what are the indications for dialysis in overload

A

nutrition

**pulmonary oedema

hypertension

47
Q

what are the indications for dialysis in uraemia

A

altered mentat status

**pericarditis

unexplained bleeding

48
Q

what is haemodialysis

A

Solute removal by diffusion

Intermittent therapy – each session lasting 3-5 hours

49
Q

what is haemofiltration

A

Solute removal by convection

Larger pore size

Continuous therapy

50
Q

what are the advantages of haemodialysis

A

Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment for hypercatabolic patient

51
Q

what are the disadvantages of haemodialysis

A

Haemodynamic instability
Concern if dialysis associated with hypotension, may prolong AKI
Fluid removal only during short treatment time

52
Q

what are the advantages of continuous RRT (i.e. haemofiltration)

A

Slow volume removal associated with greater haemodynamic stability
Absence of fluctuation in volume and solute control over time
Greater control over volume status

53
Q

what are the disadvantages of continuous RRT

A

Need for continuous anticoagulation
May delay weaning/mobilisation
May not have adequate clearance in hypercatabolic patient

URINARY (27 decks)

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