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Supporting life block > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Define Acute kidney injury (AKI)

A
  • The syndrome arising from a rapidly falling GFR
  • Characterised by retention of both nitrogenous ( e.g urea & creatinine) and non-nitrogenous waste products, as well as disordered electrolyte, acid-base and fluid homeostasis
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2
Q

When is AKI diagnosed

A
  • When serum creatinine is greater than or equal to 26.5 micromoles/l in less than or equal to 48 hours
  • or rises to greater than or equal to 1.5-fold from baseline in the preceding 7 days
  • Urine is less than 0.5ml/kg/h for 6 hours
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3
Q

How is kidney failure classified?

A

Stage 1: Creatinine rise greater than or equal to 26.5micro moles per litre in 48h OR 1.5-1.9 times from baseline
Urine output is less than or equal to 0.5ml/kg/h for 6-12h
Stage 2: Creatinine rises 2-2.9 times from baseline
Urine output is less than 0.5ml/kg/h for greater than or equal to 12 hours
Stage 3: Creatinine rise is greater than or equal to 3 times from base line OR rise to greater than or equal to 353.6 micro moles per litre OR RRT irrespective of serum creatinine
Urine output is less than 0.3ml/kg/h for greater than or equal to 24h or anuria for greater than or equal to 12h

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4
Q

What are the proximal tubular cells very susceptible to?

A

Hypotension & hypoxia

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5
Q

What percentage of CO is renal blood flow?

A

25%

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6
Q

What are some of the causes of AKI?

A
  • hypovolemia
  • Cardiac failure
  • drugs
  • renal artery occlusion
  • small vessel vasculitis
  • Tumours
  • Papillary necrosis
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7
Q

Which locations of the kidney could AKI occur?

A
  • Pre-renal
  • Renal artery
  • Small vessel disease
  • Glomerular disease
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Intra-tubular obstruction
  • Post-renal obstruction
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8
Q

What is anti-GBM disease?

A

-an antibody disease; a rare autoimmune disorder in which circulating antibodies are directed against an antigen normally present in the GBM and alveolar basement membrane

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9
Q

Where do pre-renal causes of AKI take place?

A

Renal arteries& aorta

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10
Q

Where do renal causes of AKI take place ?

A

Kidneys (cortex & medulla)

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11
Q

Where do post-renal causes of AKI take place?

A

Collecting ducts

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12
Q

How can we classify AKI causes?

A
  • pre renal
  • intrinsic (renal)
  • post renal
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13
Q

What are some causes of pre renal AKI

A
  • Volume depletion
  • Decreased effective volume
  • Altered intrarenal haemodynamics
    1. )NSAIDs
    2. ) ACEi-A2RB-induced
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14
Q

What are some causes of intrinsic AKI

A
  • Acute tubular necrosis
  • Acute glomerulonephritis
  • Acute interstitial nephritis
  • Vascular (small/large vessel)
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15
Q

What are some causes of post renal AKI

A
  • Ureteric obstruction

- Bladder outflow obstruction

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16
Q

What are the functions of kidneys ?

A
  1. ) Excretion of electrolytes
  2. ) Clearance of waste products
  3. )Receptor sites for hormones
    - ADH
    - Aldosterone
    - ANP
    - PTH
  4. ) Gluconeogenesis
  5. ) Regulation of acid-base state
  6. ) Control of water balance
  7. ) Production of hormones
    - Renin
    - Vitamin D
    - Erythropoetin
    - Prostaglandins
17
Q

What are the effects of AKI?

A
  • Fluid overload/pulmonary oedema
  • Hyperkalaemia
  • uraemia
  • metabolic acidosis
18
Q

What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of 5.5-6.5mmol/L ie early hyperkalaemia

A
  • Peaked T waves

- Prolonged PR segment

19
Q

What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of 6.5-8mmol/L

A
  • loss of p wave
  • prolonged QRS complex
  • ST- segment elevation
  • Ectopic beats and escape rhythms
20
Q

What are the possible ECG abnormalities of a hyperkalaemic serum potassium range of greater than 8 mmol/L

A
  • Progressive widening of QRS complex
  • Sine wave
  • Ventricular fibrillation
  • Asystole
  • Axis deviations
  • Bundle branch blocks
  • Fascicular blocks
21
Q

What are the typical ABGs for metabolic acidosis?

A
  • pH<7.3
  • pCO2=low
  • Po2= normal/high
  • HCO3=low
22
Q

What are the typical symptoms of metabolic acidosis?

A
  • Breathless/tachypnoeic
  • Nausea
  • Non-specifically unwell
  • The patient will hyperventilate to try get rid of the co2 and to try normalise the pH
23
Q

What is Uraemia

A
  • Retention of metabolic waste products that are otherwise excreted by the kidneys( sulphate, urea, ammonia, creatinine, phosphate etc)
  • Clinically, we measure urea and creatinine
24
Q

What are the effects of uraemia?

A
  1. ) Pericarditis: the pericardial membrane around the heart (which is normally very smooth with very little fluid) will become inflammed
  2. ) Pleurisy: Pleural effusion could occur (in between the lung& pleural membrane)
  3. ) Encephalopathy: brain disease/damage/malfunction; metabolic waste products may cause damage to the BBB and so cause lethargy,violence,comatised& change in mood/personality
25
Q

What are pericardial tamponades?

A
  • Heart stops pumping/producing BP- This could be fatal

- Compression of the heart occurs due to build up of fluid in the pericardium

26
Q

How can we manage AKI?

A
  1. ) Exclude a life threatening complication
  2. ) Identify the aetiology…
    - Hypovolemic: give fluids
    - Low BP: fluids/drugs
    - If drug induced: stop drugs
    - If sepsis induced: treat sepsis
  3. ) Supportive treatment: nutrition, ulcer prophylaxis
  4. ) Avoidance of progression: avoid nephrotoxic drugs/hypovolemia/hypotension
27
Q

When do we give Renal replacement therapy( RRT)

A

-When it is indicated that there’s a life threatening complication of AKI e.g:
-Life threatening pulmonary oedema
-Severe metabolic acidosis
-Severe hyperkalaemia, especially if ECG changes
AND the following are present
-Uraemic pericarditis
-Uraemic encephalopathy

28
Q

Outline the principle of RRT

A
  • Blood from patient goes through a blood pump and into a filter that removes water& electrolytes
  • The blood then flows through an air detector that detects any changes in air composition’
  • The blood is then returned back to the patient
  • Uses the principles of OSMOSIS; similar to a dialysis machine
29
Q

Which insertion sites do we use to obtain vascular access in RRT

A 
We use dual lumen catheters
the insertion sites are: 
-Internal jugular vein
-Femoral vein
-Subclavian vein
30
Q

Define azotenia

A

high levels of nitrogen containing compounds in the blood

Supporting life block (28 decks)

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