Toxicology Flashcards

1
Q

Opioids addiction is treated with:

A

Methadone & buprenorphine: suppress withdrawal symptoms and relieve cravings.

naltrexone (Vivitrol®):Naltrexone blocks the effects of opioids at their receptor sites in the brain and should be used only in patients who have already been detoxified

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2
Q

Early symptoms of aspirin poisoning are:

A

Ringing in the ear and blurred vision

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3
Q

Antidote for warfarin:

A

vit k (the other name of it phytomenadion)

Alternative names of Vit. K (Phylloquinone; K1;) (Menaquinone; K2;) (Menadione; K3)

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4
Q

……………….. causes mydriasis while …………….. & …………….. causes miosis aka pin point pupil

A

…cocaine…. causes mydriasis while …..Heroin… & …morphine …. causes miosis aka pin point pupil

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5
Q

For a 4 year old child, the maximum daily dose of paracetamol is:

A

1.2g

while adults: 4 g

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6
Q

is extracted from the leaves of the coca plant (Erythroxylum coca)

A

Cocaine

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7
Q

MOA of Cocaine

A
  1. indirect sympathomimetic agent, blocks the presynaptic re-uptake of serotonin and catecholamines (ie, dopamine, norepinephrine, and epinephrine) from their adrenergic receptors.
  2. “Negative inotropy”***. Sodium (Na+) channel blockade – Cocaine slows or blocks nerve conduction and acts as a local anesthetic by altering the recovery of the neuronal Na+ channels. During overdose: it manifest in ECG as prolongation of QRS complex.
  3. Increases the concentration of the excitatory amino acids glutamate and aspartate in the brain. Glutamate is the main excitatory neurotransmitter of the CNS.

**Negative inotropes weaken the heart’s contractions and slow the heart rate.

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8
Q

The euphoric properties of cocaine derive from the inhibition of neuronal ……………………………. reuptake in the central nervous system, while addiction has been linked to effects on ………………………………..

A

The euphoric properties of cocaine derive from the inhibition of neuronal serotonin reuptake in the central nervous system, while addiction has been linked to effects on dopamine reuptake

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9
Q

Heroin & Morphine

A

act at one of the 3 main opioid receptor systems (mu, kappa, delta).

Heroin is a derivative of morphine.

Opium – Opium, extracted from the opium poppy, and containing morphine and codeine.

Miosis, constipation

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10
Q

False-positive opiate drug screens have been reported in patients taking rifampin and quinolones:
True
False

A

True

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11
Q

The chemical name for heroin is

A

diacetylmorphine

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12
Q

Synthetic opioids include

A

fentanyl, tramadol, and methadone.

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13
Q

semi-synthetic opioids

A

Oxycodone and hydrocodone

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14
Q

approach to digoxin toxicity:

A

Serum levels:

The therapeutic range is 0.8 to 2 ng/mL (1 to 2.6 nmol/L). The serum digoxin concentration does not necessarily correlate with toxicity.

IV: 4 hours after the last dose

Oral: 6 hours after the last oral dose

**For an acute overdose, obtain a serum concentration measurement on presentation and approximately six hours after the ingestion

Treatment:

1.Antidote: Digibind (One vial binds approximately 0.5 mg of digoxin) Empiric treatment consists of:

10 vials of digoxin Fab fragments for adults or

5 vials for children.

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15
Q

Several electrolyte abnormalities increase patient susceptibility to the toxic effects of digoxin such as:

A

hypokalemia, hypomagnesemia, and hypercalcemia,

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16
Q

Theophylline

A

narrow clinical therapeutic index.

phosphodiesterase inhibitor

used as bronchodilator in asthmatic and treat bradycardia in newborns

acute toxicity (eg, vomiting) may occur with ingested or administered doses as low as 7.5 mg/kg

17
Q

Mechanism of Theophylline toxicity:

A

Phosphodiesterase inhibition increases levels of cyclic adenosine monophosphate which augments beta-adrenergic effects. Adrenergic hyperstimulation results in the metabolic abnormalities frequently seen with theophylline intoxication Excess catecholamines may also predispose to arrhythmias as well as contribute to hypotension through beta-adrenergic mediated vasodilatation.

18
Q

Signs of Theophylline toxicity:

A

Seizures
Hypokalemia
hyperglycemia
metabolic acidosis

19
Q

the following change color of the urine to red:

A

Rifampin

Nitrofurantoin

20
Q

Iron antidote

A

Defroxamine

21
Q

TCA (amitripy) antidote

A

NAHCO3

22
Q

ASA antodite

A

N-acetyl cysteine

23
Q

Nerve gases and organophospohorus antodote

A

Atropine followed by Pralidoxime

24
Q

OPOID antidote (morphine, Codeine, Heroin and Fentanyl)

A

NAloxone, Nalmefene

25
Q

Benzo (Diazepam) antidote:

A

Flumazenil

26
Q

beta blocker antidote

A

GLucagon

27
Q

Isoniazid antidote

A

Pyridoxine

28
Q

Anticholinergic antidote

A

physostigmine

29
Q

Cupper antidote

A

D-pencillinamine

30
Q

Thalium antidote:

A

Prussian blue

31
Q

The earliest signs of phenytoin toxicity are

A

horizontal nystagmus and unsteady gait.

More severe toxicity results in slurred speech, along with a gradually worsening mental status typified by lethargy, confusion, or coma.

32
Q

patient on benztropine, what’s the antidote?

A

Physostigmine or pyridostigmine

33
Q

Ethanol is metabolized to

A

Acetic acid

34
Q

Isopropanol “Rubbing alcohol” is metabolized to

A

Acetone (TOxic)
Leads to: Acetenemia (false elevation of Cr) and Ketosis without acidosis.

Tx: FOmepizole and dialysis

35
Q

Ethylene glycol is found in

A

Antifreeze

lead to FLuorscent urine and ECG changes :prolong QT, wide QRS)

36
Q

Antifreeze products contain:

A

Ethylene glycol

37
Q

snow storm vision is unique manifestation of ………………. toxicity.

A

Methanol (adulterated alcoholic beverage aka. Moonshine)

38
Q

Formic Acid is end product of:

A

Methanol (Moon shine)

Tx: Fomepizole + Dialysis