Lactic Acidosis Flashcards

1
Q

lactate generation

A

originates from red cells, skeletal muscle, brain and renal medulla

it is the end product of anaerobic metabolism of glucose

clearance of it requires hepatic uptake and aerobic conversion to pyruvate then glucose

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2
Q

what is the normal range for lactate

A

0.6 -1.2 mmol/L

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3
Q

what happens to lactate levels in the fasted state and during severe exercise

A

generally lowest in the fasted state

severe exercise - can rise up to 10mmol/L

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4
Q

at what lactate level is acidosis more likely

A

>5 mmol/L

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5
Q

Type A

A

associated with tissue hypoxaemia

  • infarcted tissue eg bowel
  • cardiogenic shock
  • hypovolaemic shock: sepsis (endotoxic) and haemorrhage
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6
Q

Type B

A

acidosis occuring when there is no clinical evidence of poor tissue perfusion or hypoxaemia

may occur in liver disease/leukaemic states

associated with diabetes - 10% of DKA cases have lactate >5mmol/L

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7
Q

what should one consider if lactic acidosis and patient is well and non-diabetic

A

rare inherited metbolic condition

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8
Q

metformin and lactic acidosis

A

metformin can cause lactic acidosis in severe illness states or renal failure

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9
Q

clinical features

A

hyperventilation - trying to restore metabolic acidosis by breathing off CO2

mental confusion

stupor/coma if severe

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10
Q

lab findings

A

reduced bicarbonate

raised anion gap

glucose variable

absence of ketonaemia

raised phosphate

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11
Q

anion gap

A

[(Na+ + K+) – (HCO3 + Cl-)]

estimates unmeasured plasma anions (fixed/organic acids such as phosphate, ketones and lactate, which are hard to measure directly)

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12
Q

raised anion gap

A

Due to increased production, or reduced excretion of fixed/organic acids. HCO3- falls and unmeasured anions associated with the acids accumulate.

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13
Q

causes of raised anion gap

A

ketones (DM/alcohol)

uraemia (renal failure)

lactic acid (shock, infection, tissue ischaemia)

starvation

drugs/toxins (ethylene glycol, methanol, salicylate or paraldehyde poisoning)

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14
Q

treatment

A

underlying condition: fluids and antibiotics

withdraw offending medication

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15
Q

alcohol ketoacidosis

A

metabolic complication of alcohol use and starvation characterised by hyperketonaemia and raised anion gap metabolic acidosis without significant hyperglycaemia

  • alcohol diminishes hepatic gluconeogenesis which causes less insulin to be produced. the body breaks down fats for energy and produces ketones as by-products
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16
Q

clinical features of AK

A

nausea, vomiting and abdominal pain

17
Q

diagnosis of AK

A

history and findings of ketoacidosis without hyperglycaemia

18
Q

treatment of AK

A

pabrinex: high dose vitamins

IV fluids: dextrose

on occasion insulin is required

address alcohol dependency