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IPT: CC > Block 3 More, why?? > Flashcards

Block 3 More, why?? Flashcards

1
Q

What is the poison control number?

A

1-800-222-1222

or text POISON to 797979

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2
Q

Sympathomimetic toxidromes are caused by what? Tx?

A

Caused by caffeine, cocaine, amphetamines, alcohol/drug withdrawal

Tx = BZD

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3
Q

Cholinergic toxidromes are caused by what? Sx?

A

Cholinesterase inhibitors, nerve gas, pesticides

SLUDGE

Salivation, lacrimation, urination, diarrhea, GI distress, emesis

Muscarinic + Nicotinic effects

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4
Q

Anticholinergic toxidromes are caused by what? Sx? Tx?

A

Diphenhydramine, OAB rx, Atropine, glypyrollate

Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, and heart runs alone

Tx = BZD or physostigmine (dont use if you dont know what rx went in)

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5
Q

What does RADAR stand for?

A 
Recognition
Assessment
Definitive Diagnosis
Advice
Reporting
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6
Q

PR prolongation
QRS prolongation
QTC prolongation

Antidepressants
Non DHB CCB
TCAs

Which Rx cause the AE?

A

TCA - QRS prolongation

Antidepressants - QTC prolongation

Non DHB CCB - PR prolongation

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7
Q

Anion Gap elevations is due to what?

A

Methanol, propylene glycol, ethylene glycol, salicylate

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8
Q

SDT vs UDS, which one provides quantitative values?

A

SDT

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9
Q

What are some poor candidates to use with activated charcoal?

A

Inorganic
Polar
Charged
Can only adsorb to something in dissolved liquid phase

PHAILS

Pesticides, hydrocarbons, acids/alkali, iron, lithium, solvents

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10
Q

Single and multiple dosing strategy for activated charcoal?

A

Single = 1mg/kg

Multiple = 0.25-0.5mg/kg every 1 to 6 hrs

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11
Q

Activated charcoal CI?

A

Pt in stupor phase, coma, convulsing unless they have endotracheal tube

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12
Q

Who should get whole bowel irrigation?

A

Any delayed/sustained release products

Large amounts of metal

Xenobiotics w/ slow absorption phase

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13
Q

Hemodialysis is beneficial for xenobiotics that have..

Low or High Vd
Single or multiple PK parameters
Low or high protein binding capacity
Small or High weight
Water soluble or insoluble
A 
Low Vd (<1L/kg)
Single PK
Low protein
Small weight (<5000 Daltons)
Water soluble
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14
Q

What class do organophosphates and carbamates belong to?

A

Cholinesterase inhibitors

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15
Q

What groups are found in the organophosphates and carbamates?

A

Organo - oxygen + leaving group that attaches to O2 or phosphorous + 2 side chains

Carbamates - N methyl group + NCOO

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16
Q

How do you manage organophosphate toxicity?

A

BZD for seizures

Atropine (only works on ACh receptors); so no effect on paralysis, fasciculations

Alternatives to atropine: glycopyrrolate (only works for periphery), ipratropium, scopolamine

Pralidoxime (2-PAM), give atropine prior

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17
Q

How does pralidoxime (2-PAM) work?

A

It attaches the N-OH group to the organophosphate’s P group (where the R20 was)

18
Q

Kappa receptor is responsible for what action of opioids?

A

Miosis + sedation

19
Q

Mu1 receptor is responsible for what action of opioids?

A

Analgesia, everything else is Mu2

20
Q

Which opioid lowers seizure threshold?

A

Tramadol

21
Q

Tramadol interacts with what Rx?

A

Antidepressant meds

22
Q

Tramadol is a (mu/kappa) agonist. Oxycodone..?

A

Tramadol - mu

Oxycodone - both

23
Q

Which opioids are metabolized by CYP2D6?

A

Codeine + Tramadol

24
Q

Tolerance to _________ develops slower than analgesia and euphoria for opioids

A

Respiratory depression

25
Q

RF for opioid overdose?

A

> 50MME/day

> 90 days of use

26
Q

Naloxone is a (mu/kappa) antagonist

A

Mu antagonist

27
Q

Protein binding and acceptable ranges of APAP and NSAIDs?

A

APAP - low protein, 10-30

Aspirin - high protein, 15-30

Other NSAIDs - high protein, doesnt say :/

28
Q

Metabolism of APAP

A

Most go through non CYP metabolism

Small % goes through CYP2E1 which forms NAPQI, which glutathione attaches to. In overdose situations, glutathione is depleted and NAPQI attaches to hepatocytes

29
Q

Staging of APAP toxicity?

A

1 = no hepatic damage, basic AE, days 0-1

2 = AST/ALT >1000, URQP, 5% of cases, days 1-3

3 = AST/ALT >10,000, hepatic failure, danger zone for death is days 3-5

4 = recovery

30
Q

Limitations of Rumack-Matthew Nomogram?

A

No guidelines for <4hrs

Altered mental status or patient history is too unreliable to plot correctly

Limited evidence in children

Limited evidence in ER formulation

31
Q

Aspirin toxicity AE?

A

Inhibits the citric acid cycle - Metabolic acidosis

Uncouples oxidative phosphorylation - Ketoacidosis

Direct stimulation of the respiratory center - Respiratory alkalosis

32
Q

Clinical triad of ASA toxicity?

A

Hyperventilation
Tinnitus (cochlear toxicity)
GI irritation

33
Q

What are the non-DHP CCB?

A

Verapamil + Diltiazem

34
Q

(DHP/Non-DHP CCB) inhibit both SA + AV nodes. What does the other one do primarily?

A

Non-DHP

Tends to act as a peripheral vasodilator

35
Q

In the event of a CCB overdose, how is insulin affected?

A

Less insulin release

36
Q

Can you use dialysis on CCB overdose?

A

No, they are highly protein bound

37
Q

Non DHP CCB toxic effects

A

Bradycardia

Hyperglycemia

Lactate production + metabolic acidosis

38
Q

DHP CCB toxic effects

A

Reflex tachycardia

Higher doses, bradycardia

39
Q

Treatment option for Non DHP CCB or BB?

A

Activated charcoal, maybe more better for XR formulation

Atropine (treats bradycardia)
Glucagon (increases adenylate cyclase)
Calcium chloride/gluconate
Sodium bicarb (for QRS, not for urine alkalization) 
Vasopressors
High dose insulin
IV fat emulsion
40
Q

Digoxin toxicity AE?

A

Bradycardia

Hyperkalemia

Arrhythmias

41
Q

Digoxin toxicity treatment?

A

Activated charcoal, even past the 1-2hr mark

Atropine

DigiFab (40mg reverse 0.5mg of digoxin)

42
Q

Can you use BB for cocaine overdose?

A

No

Just treat with ASA, O2, BZD, nitroglycerin

IPT: CC (7 decks)

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