Toxicology Flashcards

(30 cards)

1
Q

Why does hepatic damage occur?

A

Liver glutathione store becomes deplete
Glutathione usually protects hepatic cells from oxidative damage

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2
Q

What condition would glutathione stored be reduced?

A

Anorexic

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3
Q

How is paracetamol metabolised?

A

Conjugation forming paracetamol glucuronide and sulphate
Oxidation forming NAPQI

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4
Q

How does the treatment with acetylcysteine relate to clinical outcome?

A

If given more than. 8 hours after ingestion there is.a 5.3% death from hepatic failure

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5
Q

Why are blood glucose levels low following paracetamol overdose?

A

Livers ability to breakdown glycogen is reduced

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6
Q

Why does paracetamol overdose result in elevated levels of toxic metabolite?

A

The conjugation pathway becomes saturated converting paracetamol into NAPQI

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7
Q

What are biochemical and haematological abnormalities seen in paracetamol poisoning?

A

AST, ALT, Bilirubin and amylase increase
Blood sugar, phosphate,platelets decrease

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8
Q

What organs does NAPQI damage?

A

Liver and kidneys

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9
Q

What is the AST/ALT value given for severe hepatic damage?

A

1000IU/L

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10
Q

Why is there a metabolic acidosis?

A

Massive indigestion
Hepatic failure
Shock  Hypoperfusion  Anerobic respiration

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11
Q

How is acetylcysteine administered?

A

IV for 21 hours

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12
Q

What are the antidotes to paracetamol poisoning?

A

Glutathione percursors

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13
Q

What is the most common paracetamol antidote?

A

Acetylcysteine

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14
Q

What substance does NAPQI alter the regulation of?

A

Calcium

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15
Q

Why is INR increased and platelet levels decreased in paracetamol overdose?

A

Hepatic failure causes reduction in anti thrombin
More thrombin causes DIC
DIC use up all platelets

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16
Q

When do adverse events occur in AC administration?

A

Immediately after the initial bolus dose

17
Q

Why does phosphate decrease in paracetamol poisoning?

A

Livers ability to breakdown glycogen is reduced

18
Q

How is NAPQI removed?

A

Conjugated with glutathione- forming cysteine and mercapturate conjugates

19
Q

Possible adverse event associates with acetylcysteine?

A

Flushing
Urticaria
Puritus
Bronchospasm

20
Q

Physical properties of carbon monoxide that render it difficult for humans to detect?

A

Non irritating, colourless, odourless gas
No physiological trigger

21
Q

How is exogenous carbon monoxide formed?

A

Formed during incomplete combustion of carbon fuels

22
Q

Where might carbon poisoning occur?

A

Car exhaust in garage
Older properties with unmaintained heating systems
Blocked chimneys above wood or gas fires
Presence with other toxins

23
Q

How and why does Co poisoning cause tissue hypoxia?

A

Binds to Haemoglobin
Causes a decrease in arterial O2 content and shift of the oxyhemoglobin dissociation curve to the left
Oxygen not delivered to organs or tissues

24
Q

Symptoms of carbon monoxide poisoning?

A

Headache
Dizziness and nausea
Vomiting
Tiredness and confusion
Stomach pain
Difficulty breathing

25
What gives the cherry red appearance to the skin of a CO poisoned individual?
Formation of COHb seen in 2-3% of individuals post mortem
26
What organs are particularly sensitive to carbon monoxide poisoning and why?
Heart and brain because they are oxygen hungry
27
What is the mechanism of toxicity in the heart?
CO binds to myoglobin with high affinity thus reducing the oxygen supply to the mitochondria. CO affects oxidative phosphorylation and therefore the energy source to the myocardium. Lipid peroxidation results from increased free radical production in the presence of NO to peroxynitrite Lactic acidosis results from anaerobic metabolism of the cells.
28
What diagnostic test is performed to confirm carbon monoxide poisoning?
Spectrophotometer is analysis of arterial blood for COHb is the quantitative test Also kunkels test, pulse oximetry, PO2, lactate levels
29
What is the normal treatment following suspected/confirmed CO poisoning?
Atmospheric O2 concentration 100% ocygen given through a non-rebreather mask Hyperbaric oxygen treatment
30
Conditions where hyperbaric treatment might be required?
Pregnant Pre-existing heart conditions Respiratory insufficiency Individuals who have lost consciousness Evidence of neurological affects Hugh COHb levels >40%