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Pharmacists Hate Him > Toxicology > Flashcards

Toxicology Flashcards

Learn about drugs, don't do drugs. -Mike 2022

1
Q

What is the generalized mechanism of direct-action cholinergic drugs?

A

Bind to cholinergic receptors, stimulating the organ in a similar way as ACh

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2
Q

What is the generalized mechanism of indirect-action cholinergic drugs?

A

Inhibit the enzyme ‘acetylcholinesterase,’ resulting in more ACh available at the receptors

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3
Q

Between direct and indirect-action cholinergic drugs, which category is best suited for treating Alzheimer’s?

A

Indirect-action:
More sustained levels of ACh in the nervous system leads to improved neurotransmission

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4
Q

What does the “S” in “SLUDGE M” stand for?

A

Salivation

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5
Q

What does the “L” in “SLUDGE M” stand for?

A

Lacrimation

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6
Q

What does the “U” in “SLUDGE M” stand for?

A

Urination

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7
Q

What does the “D” in “SLUDGE M” stand for?

A

Diaphoresis

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8
Q

What does the “G” in “SLUDGE M” stand for?

A

Gastrointestinal Discomfort

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9
Q

What does the “E” in “SLUDGE M” stand for?

A

Emesis

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10
Q

What does the “M” in “SLUDGE M” stand for?

A

Miosis (Pupil constriction)

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11
Q

Three FDA-approved cholinergic drugs for treating Alzheimer’s

A

Donepezil, Rivastigmine, Galantamine

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12
Q

Common causes of cholinergic toxicity

A

Exposure to insecticides or military nerve agents

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13
Q

Why does cholinergic toxicity cause sweating (a sympathetic response)?

A

ACh acts on muscarinic receptors of sweat glands

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14
Q

What is ACh?

A

Neurotransmitter for PNS and SNS

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15
Q

What are some treatments for cholinergic toxicity as per ALS PCS?

A

Atropine, Pralidoxime, Diazepam

(Pralidoxime is the main antidote used in definitive care)

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16
Q

Why is seizure activity/muscle twitching common in cholinergic toxicity?

A

Increased ACh in synapses means increased nervous system excitability

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17
Q

What is the mechanism of action of anticholinergic drugs?

A

Anticholinergic drugs block the muscarinic and nicotinic receptors so that ACh cannot act on them

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18
Q

What toxidrome causes a “wet” patient?

A

Cholinergic

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19
Q

What toxidrome causes a “dry” patient?

A

Anticholinergic

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20
Q

What are the key signs of anticholinergic toxicity?

A

-Red, hot, dry skin
-Tachycardia
-Dry mouth
-Constipation
-Mydriasis (Pupil dilation)
-Blurred vision
-Altered LOA

21
Q

What are some examples of anticholinergic drugs?

A

-Diphenhydramine (Allergic reactions, sleep aid)
-Dimenhydrinate (N/V, motion sickness)
-Atropine (Given by ACPs to treat bradycardia)
-Atrovent (Bronchodilator used to treat COPD)
-Scopolamine (N/V, motion sickness, commonly used by SCUBA divers thru transdermal patches to aid with seasickness)
-TCAs (Uncommon anti-depressant, stupid easy to OD on)
-Antipsychotics (It lives in my drywall)
-Jimson Weed (silly flower that is smoked for hallucinogenic properties)

22
Q

What is considered a lethal dose of TCAs?

A

10-20mg/kg

23
Q

What is the mechanism of action found in a TCA overdose?

A

Loss of vascular tone following muscarinic and alpha receptor blockage. Sodium channel is also blocked, leading to signature prolonged QT intervals.

24
Q

What are the signs and symptoms of a TCA overdose?

A
  • Hx of TCA use
  • Red, hot, dry skin
  • Tachycardia
  • Loss of bowel sounds (If you insist, Mike)
  • Prolonged QT intervals with risk of lethal arrhythmia
25
Q

What is the difference between QT interval and QTc on a cardiac monitor?

A

QT interval changes naturally depending on HR, QTc adjusts based on heart rate to determine the true measurement of QT interval

(QTc should be used to determine if QT interval is prolonged)

26
Q

What is considered a prolonged QTc?

A

Anything greater than 0.44s

27
Q

What is the mechanism of action responsible for opioid overdoses?

A

Opioids bind to chemoreceptors and render them less sensitive, slowing the respiratory drive

28
Q

What is the antidote for opioid overdose?

29
Q

What is the mechanism of action of Naloxone?

A

Naloxone kicks the opioids off chemoreceptors, allowing for a return to normal respiratory drive once receptors notice the elevated CO2 in blood.

30
Q

Is naloxone an opioid agonist or antagonist?

A

Antagonist

31
Q

Give a few examples of opioid agonists

A
  • Fentanyl (80x more potent than morphine)
  • Morphine (Reduces sensation of pain)
  • Methadone (All the effects of morphine minus the euphoria, used for cessation treatment)
  • Crocodil (Desomorphine) (Simply had to be mentioned)
  • Heroin
  • Demerol
32
Q

What is unique about a Demerol overdose?

A

Pupils will remain unaffected

33
Q

What are the signs and symptoms of an opioid overdose?

A
  • Miosis
  • Decreased respiratory drive
  • High ETCO2
  • Altered LOA
  • Hx of opioid use, paraphernalia on scene
34
Q

How does the half-life of naloxone compare to most opioids?

A

Naloxone typically has a shorter half-life than most opioids, meaning naloxone may wear off before opioids are flushed from system

35
Q

Typical half-life of naloxone

A

10 mins - 2 hours

36
Q

What is unique in a methadone overdose?

A

Methadone has a very long half-life, meaning naloxone infusions will need to be carried on in definitive care

37
Q

What is the mechanism of action of sympathomimetic drugs?

A

They either cause the release of norepi OR prevent it’s reuptake

38
Q

What are some common sympathomimetics?

A
  • Cocaine
  • Methamphetamines (Jesse, we need to cook)
  • Caffeine (yes, please)
  • Decongestants
  • Ephedrine (used to treat hypotension in patients undergoing anesthesia)
39
Q

What are the signs and symptoms of a sympathomimetic overdose?

A
  • Pallor
  • Diaphoresis
  • Miosis
  • N/V
  • Present bowel sounds
  • Altered LOA/ psychosis
  • Seizures/Tremors
  • Cardiac dysrhythmias
40
Q

How does a sympathomimetic overdose compare to anticholinergic toxidrome?

A

Anticholinergic toxidromes:
- Dry, flushed skin
- No bowel sounds
- Hx of anticholinergic use

Sympathomimetic ODs:
- Pale skin
- Diaphoresis
- Present bowel sounds
- Hx of sympathomimetic use

41
Q

Why do sympathomimetic toxidromes present with diaphoresis and bowel sounds whereas anticholinergic toxidromes do NOT?

A

Anticholinergics prevent ACh from acting on the muscarinic receptors of sweat glands and GI tract whereas sympathomimetics do not affect ACh binding. They instead cause the SNS to act a fool due to increased norepi / epi

42
Q

What is piloerection?

A

Goosebumps (get your head out of the gutter, son)

43
Q

What is the most common cause of serotonin toxicity?

A

The combination of two serotonin elevating drugs that operate via two different mechanisms of action OR increased doses of serotonin-elevating drugs (anti-depressants)

44
Q

What is the trifecta of serotonin toxicity SS?

A

Altered LOA:
- Anxiety
- Restlessness
- Agitation
- Hallucinations

Neuromuscular Hyperactivity:
- Akathisia (inability to sit still)
- Tremors
- Hyperreflexia
- Clonus (muscles randomly contracting)

Autonomic Hyperactivity:
- Increased BP
- Tachycardia
- Tachypnea
- N/V/D
- Mydriasis
- Diaphoresis

45
Q

What is one of the most dangerous drug withdrawals?

A

Alcohol withdrawal that is accompanied by DTs

46
Q

What is the patho of alcohol withdrawal?

A

The body is used to being very CNS heavy to compensate for the CNS depressing factors of alcohol. When the alcohol is no longer in the picture, the elevated CNS becomes apparent which leads to the negative (life threatening) effects.

47
Q

What are some SS of benzo OD?

A

Decreased LOA with normal vitals, supportive care is often all that is needed.

48
Q

How long does it typically take for acetaminophen OD symptoms to become apparent?

A

18-24 hours

49
Q

What are the SS of acetaminophen OD?

A

RUQ pain, hypotension, liver/renal failure, metabolic acidosis

Why?
RUQ is where liver pain is referred

Liver failure is caused by metabolic process

Metabolic acidosis is caused by renal/liver damage causing inability to filter blood / maintain pH

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