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EDIC academy > AKI (Part V) > Flashcards

AKI (Part V) Flashcards

1
Q

Fluid administration in sepsis as per surviving sepsis guidelines?

A

At least 30ml/kg

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2
Q

Risk & benefits of administration of normal saline?

A
  • Hyperchloremic acidosis
  • Beneficial in traumatic brain injury
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3
Q

Action of Furosemide on the kidney?

A
  • Renal protection by decreasing renal tubular oxygen demand
  • Expedites renal function recovery by washing out necrotic debris blocking the tubule
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4
Q

RBF ?

A
  • It is constant due to autoregulation
  • Dependent on arterial blood pressure
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5
Q

Norad?

A
  • Alpha and beta agonist effects
  • Increases contractility
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6
Q

Adrenaline?

A
  • Increases CO & perfusion pressures
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7
Q

Metabolic side effects of Adrenaline administration?

A
  • Hyperglycaemia
  • Acidosis
  • Hyperlactataemia
  • Deleterious effect on splanchnic circulation
  • Proarrhythmogenic
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8
Q

Dopamine?

A
  • Dopaminergic effect - Direct renal vasodilation
  • Stronger beta effect
  • Not recommended in septic shock
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9
Q

Phenylephrine ?

A
  • Synthetic pure alpha agonist
  • No beta effect
  • Effect is dependent on preload status
  • Induces increased venous resistance
  • increases CO only
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10
Q

Vasopressin?

A
  • Potent vasopressor
  • Action on the mesenteric compartment
  • Pure vasoconstrictor w/o inotropic effect
  • Useful in septic shock
  • May prevent progression of AKI
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11
Q

Vasopressin deficiency ?

A
  • Septic shock induced reduced vascular tone
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12
Q

Effects of various vasopressors?

A

See attached image

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13
Q

Drugs to avoid in order to prevent AKI?

A
  • NSAIDs
  • ACE inhibitors
  • ARBs
  • Contrast agents
  • Aminoglycosides
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14
Q

What is the chemical name for statins ?

A

3-hydroxy-3-methylglutaryl-CoA reductase inhibitor

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15
Q

Useful effects of statins?

A
  • Anti-inflammatory
  • Endothelial stabilizer
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16
Q

What are the hallmarks of critical illness?

A
  • Alteration in fluid status
  • Absolute volume depletion (Hypovolaemic or haemorrhagic)
  • Relative volume depletion ( page 9
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17
Q

How does renal blood flow remain constant?

A

Autoregulation

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18
Q

What does renal blood flow depend on ?

A

Arterial pressure

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19
Q

What is the target MAP for patients with chronic HTN?

A

80-85mmHg as this is renal protective and reduces the need for RRT

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20
Q

Are alpha-receptors present in the renal vessels?

A

Their density here is relatively high

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21
Q

What occurs when the MAP is below the autoregulatory threshold ?

A

Increasing the MAP will directly increase Renal Blood Flow

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22
Q

What does the threshold and slope of the autoregulatory curve depend on?

A

Comorbidities;
- HTN
- Vascular disease

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23
Q

What is the target MAP for critically unwell patients?

A

This depends on the prior presence or absence of chronic HTN

24
Q

What are the effects of vasopressors on renal vasculature?

A
  • Increases MAP & RBF
  • Glomerular filtration - Effect on afferent & efferent arterioles
25
Q

Effects of vasoactive drugs

A

See attached image

26
Q

Effects of vasopressors?

A

See attached image

27
Q

What are the effects of Norepinephrine?

A
  • Alpha-agonist
  • Beta-agonist
  • Increased contractility
28
Q

What are the effects of epinephrine?

A
  • Increased CO & perfusion pressures
29
Q

What are the metabolic side-effects of epinephrine (Adrenaline)?

A
  • Hyperglycaemia
  • Hyperlactataemia
  • Acidosis
  • Pro-arrhythmogenic
  • Impairment of splanchnic circulation
30
Q

Effect of low dose Dopamine?

A
  • Direct renal vasodilation
31
Q

Properties of Dopamine ?

A
  • Weak vasoconstrictor effect
  • Predominant Beta-effect
  • Not recommended for sepsis
32
Q

Properties of phenylephrine?

A
  • Pure alpha-agonist
  • Effect depends on preload & LV function
33
Q

Characteristics of Vasopressin?

A
  • Potent vasopressor
  • It is non-catecholamine
  • Pure vasoconstrictor
  • No inotropic effect
  • Prevents progression of AKI
34
Q

What is the relationship between septic shock and vasopressin?

A
  • During septic shock there might be vasopressin deficiency
  • Decrease in vessel tone
35
Q

Review vasoactive drugs alongside their renal and systemic effects ?

A

See image attached

36
Q

Nephrotoxic drugs to avoid?

A
  • NSAIDs
  • Contrast
  • ACEi / ARBs
  • Aminoglycosides
37
Q

What is the full name for statins?

A

3-Hydroxy-3-Methylglutaryl-CoA reductase inhibitor

38
Q

What are the effects of statins?

A
  • Lowering cholesterol levels
  • Anti-inflammatory
  • Endothelial stabilization
39
Q

Major mechanisms of development of AKI?

A
  • Inflammatory pathways
  • Endothelial dysfunction
40
Q

Characteristics of iodinated contrast agents ?

A
  • Iso-osmolality
  • Reduced risk of AKI
41
Q

Alkaline phosphatase?

A
  • Endogenous enzyme
  • Detoxifying effect
  • Renoprotective effect
42
Q

Nephrotoxicity can be caused by ?

A
  • Hyperglycaemia
43
Q

Resuscitation using goal directed therapy ?

A

See image attached

44
Q

What are the absolute indications for RRT ?

A
  • Hyperkalaemia
  • Metabolic acidosis
  • Pulmonary oedema
  • BUN > 140mg/dL
  • Pericarditis
45
Q

Furosemide stress test ?

A
  • High sensitivity & specificity
  • Predicts progression of AKI
46
Q

Conditions potentiating the harmful effect of hyperkalemia?

A
  • Acidosis
  • Hypocalcemia
  • Hyponatremia
47
Q

Systemic effects of hyperkalemia ?

A
  • Muscle weakness
  • Shortened QT interval
  • Tall T-waves
  • Progressive lengthening of QRS & PR intervals
  • VF is a possibility
48
Q

What is the role of B2-Adrenergic agonist in Mx hyperkalemia ?

A
  • Acts directly on Na/K-ATPase
  • Avoid in individuals with coronary disease
48
Q

What is the role of calcium chloride/gluconate in hyperkalemia?

A
  • Antagonizes cardiac membrane excitability and onset of effect is within minutes.
  • Beneficial when ECG changes are present
48
Q

What is the role of insulin in hyperkalemia ?

A
  • Stimulates Na/K-ATPase activity
  • Shift of potassium into the cell
  • Approx. 0.5-1.5mmol/L fall in potassium within 15 mins & peak effect observed in about 60 mins
49
Q

What is the typical ECG for hyperkalemia?

A

See image attached

50
Q

What are the causes of metabolic acidosis in AKI?

A
  • Increased acid production
  • Increased acid retention
  • Decreased bicarbonate reabsorption
51
Q

Uraemic complications ?

A
  • Observed in 10% of patients with ESRF
  • It is rarely encountered in AKI
  • ## Inflammation of visceral & parietal membrane of pericardial sac
52
Q

What is the characteristic presentation of pericarditis in AKi?

A
  • Fever
  • Pleuritic chest pain
  • Unable to lay flat
  • Pericardial rub
53
Q

What are the early clinical signs of uremic encephalopathy?

A
  • Rambling speech
  • Disorientation
  • Lethargy
  • Irritability
  • Hallucination
  • Coma
54
Q

What are the commonly encountered signs of encephalopathy ?

A
  • Tremors
  • Myoclonus
  • Asterixis

EDIC academy (19 decks)

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