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PATH 407 > Alcohols and Glycols > Flashcards

Alcohols and Glycols Flashcards

1
Q

What are the sources of methanol?

A

Windshield washer fluid
Gasoline antifreeze

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2
Q

What is the lethal methanol dosage?

A

15 mL of 40% methanol ➔ death
4 mL of 100% methanol ➔ blindness

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3
Q

How is methanol metabolized?

A

Methanol ➔ (ADH) ➔ formaldehyde (rate-limiting)
Formaldehyde ➔ (ALDH) ➔ formic acid (rapid)
Formic acid ➔ (Folate) ➔ CO2 + H2O

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4
Q

Why does methanol cause metabolic acidosis?

A
  1. Methanol is metabolized to formic acid which accounts for much of the anion gap metabolic acidosis
  2. Formic acid binds to iron & inhibits mitochondrial cytochrome c oxidase causing lactic acidosis
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5
Q

What is the clinical presentation of methanol poisoning?

A

1st few hrs
- Mild inebriation, gastritis

12-24 h
- Mild CNS depression
- Hyperventilation secondary to acidosis
- Visual disturbance: looking into snow storm, permanent visual loss can occur
- Severe cases: severe acidosis, coma, and CV collapse
- Survivors may develop Parkinson’s

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6
Q

What is the treatment of methanol?

A
  1. Inhibition of metabolism
    - Ethanol and fomezipole inhibit ADH preventing further production of formic
  2. Removal of parent compound (dialysis) - MAIN treatment
  3. Adjunctive therapy - folinic or folic acid
  4. Treatment of acidosis - sodium bicarbonate
    - bicarbonate shifts equilibrium in favor of folate
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7
Q

How safe is ethanol vs fomezipole?

A

Ethanol any ADE - 57%
Ethanol severe ADE - 11%

Fomezipole any ADE - 12%
Fomezipole severe ADE - 2%
Bradychardia and hypotension (uncommon)

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8
Q

What is the definitive diagnostic test of methanol? What are the cons of this test?

A

Gas chromatography
1. Time consuming
2. Expensive
3. Not readily available

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9
Q

What are the screening tests of methanol?

A
  1. POC test
    - Immunochromatographic test
    - Cut off for +ve test - 4 mmol/L
    - Methanol test may cross react with ethanol
  2. Osmole gap
    - Normal < 10 mOsm/L
    - Serum osmolality must be measured with an osmometer using FREEZING POINT DEPRESSION
    - only parent cmpd will increase the osmole gap
  3. Anion gap
    - Normal 7+/-4
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10
Q

What is the sensitivity and specificity of osmole gap?

A

Sens - moderate-high
Spec - low

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11
Q

What are some lab testing issues that can result in an increased osmole gap?

A
  1. Anticoagulants in collection tube
  2. Lab tests not taken simultaneously
  3. Delay in analysis
  4. Use of VAPOUR PRESSURE osmometry
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12
Q

What is the mnemonic used for an increased osmole gap?

A

MEDIE
M - Methanol
E - Ethanol
D - Diuretics
I - Isopropyl Alcohol
E - Ethylene glycol

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13
Q

What is the sensitivity and specificity of anion gap measurement?

A

Sens - low
Spec - high

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14
Q

What is the mnemonic for elevated anion gap?

A

CATMUDPILES
C - Carbon monoxide, cyanide
A - Acetaminophen, Alcohol ketoacidosis
T - Toluene
M - Metformin, methanol
U - Uremia
D - Diabetic ketoacidosis
P - Propylene glycol
I - Iron, isoniazid
L - Lactic acidosis
E - Ethylene glycol
S - Salicylates

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15
Q

What are the toxins that can increase both osmole and anion gap? (4)

A
  1. Methanol
  2. Ethylene glycol
  3. Diethylene glycol
  4. Propylene glycol
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16
Q

What are the medical conditions that can increase both OG and AG? (4)

A
  1. Alcoholic and diabetic ketoacidosis
  2. Renal failure
  3. Multiple organ failure
  4. Critical illness
17
Q

What are the sources of ethylene glycol?

A

Antifreeze
Industrial solvent

18
Q

What is the lethal EG dose?

A

1-2 mL/kg
1 swallow = 30 mL

19
Q

What is the metabolism of ethylene glycol?

A

Ethylene glycol ➔(ADH)➔ glycoaldehyde
Glycoaldehyde➔(ALDH)➔ glycolic acid
Glycolic acid ➔ glycoxylic acid ➔ oxalic acid

20
Q

What is the pathophysiology of ethylene glycol?

A

Parent cmpd is non-toxic

Toxicity of EG due to combination of severe metabolic acidosis caused by glycolic acid and the ppt. of calcium oxalate crystals resulting in impaired organ fcn esp. the kidneys.

21
Q

What is the clinical presentation of EG?

A
  1. Initial CNS depression
  2. After 4-12 h ➔ metabolic acidosis
  3. Renal failure
  4. Hypocalcemia w tetanic contractions
  5. Multiorgan failure
  6. Survivors ➔ permanent renal failure requiring dialysis
22
Q

What is the treatment for EG?

A
  1. Inhibition of metabolism ➔ ethanol & fomezipole (antidote)
  2. Removal of parent cmpd ➔ dialysis (main treatment)
  3. Adjunctive therapy ➔ pyridoxine, thiamine
  4. Treatment of acidosis ➔ sodium bicarbonate
23
Q

What is the definitive diagnostic test for EG?

A

Gas chromatography

24
Q

What are the screening tests for EG?

A
  1. Lactate gap
    - In EG poisoning, the glycolate metabolite may be interpreted as lactate on some blood analyzers. This will cause a false +ve lactate elevation on the blood gas analysis. There will be a gap between the lactat on the blood gas and the lactate determine by standard lab analysis of blood chemistry. Only works if analyser is a Radiometer ABL 700 POC analyser.
  2. Urine crystals
    - Calcium oxalate monohydrate and dihyrdrate crystals in urine. Spindle and envelope shaped respectively.
  3. Osmole gap and Anion gap (main)
25
Q

What is the toxicity of diethylene glycol vs propylene glycol?

A

Diethylene:
Resembles EG
Renal failure normally permanent ➔ lifelong dialysis
Neuropathy common

Propylene:
Low toxicity
Coma
Seizures in massive exposures or high risk patients

26
Q

What is the pathophysiology of alcoholic ketoacidosis?

A
  1. Decreased oral intake
  2. Depletion of glycogen stores
  3. Increased levels of glucagon, decreased insulin
  4. Breakdown of FA into acetyl CoA
  5. Binding of acetate (from metabolism of ethanol) to acetyl CoA ➔ acetoacetate + beta-hydroxybutyrate
27
Q

How to diagnose alcoholic ketoacidosis?

A

Increased AG, OG and serum ketones

28
Q

Why may the urine nitroprusside test for ketones in diabetic ketoacidosis turn out -ve?

A
  1. Nitroprusside rxn only detects molecules containing a ketone moiety
  2. Acetone and acetoacetate are ketone but beta-hydroxybutyrate is not
29
Q

What are the clinical manifestations of diabetic ketoacidosis?

A

Large OG ➔ increase in acetone (ketone)

Increased AG metabolic acidosis occurs in patients with ketoacidosis secondary to increased FA breakdown, protein breakdown and impaired renal function

30
Q

What are the symptoms of ethanol poisoning?

A

A - Loss of airway control
B - Respiratory compromise
C - Consciousness (decreased level)

31
Q

How to diagnose for ethanol poisoning?

A

Measure ethanol level
Increased OG but normal AG

32
Q

How is isopropyl alcohol metabolized in the body?

A

Isopropanol ➔ acetone

33
Q

What are the clinical manifstations of isopropyl alcohol poisoning?

A

CNS depression
Ketosis, FRUITY BREATH ODOR
Abdominal pain
Hypotension & resp failure after large ingestions

34
Q

How to diagnose for isopropyl alcohol poisoning?

A

Increased OG normal AG
Urinalysis - ketones present

Pseudo-renal failure

35
Q

Why may pseudo-renal failure present itself in isopropyl alcohol poisoning?

A

Increased creatinine but normal urea caused by interference of the assay for creatinine by acetone

36
Q

What is the treatment used for isopropyl alcohol poisoning?

A

Supportive care (main)

Fluids & vasopressors for hypotension
Intubation & ventilation for respiratory depression

PATH 407 (7 decks)

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